What is the most common food allergy in uk

Food

Main article: Food allergy

Name Potential reaction(s) Remarks
Balsam of Peru Redness, swelling, itching, allergiccontact dermatitis reactions, stomatitis (inflammation and soreness of the mouth or tongue), cheilitis (inflammation, rash, or painful erosion of the lips, oropharyngealmucosa, or angles of their mouth), pruritus, hand eczema, generalized or resistant plantardermatitis, rhinitis, conjunctivitis, and blisters.

Present in numerous foods, such as coffee, flavored tea, wine, beer, gin, liqueurs, apéritifs (e.g. vermouth, bitters), soft drinks including cola, juice, citrus, citrus fruit peel, marmalade, tomatoes and tomato-containing products, Mexican and Italian foods with red sauces, ketchup, spices (e.g. cloves, Jamaica pepper (allspice), cinnamon, nutmeg, paprika, curry, anise, and ginger), chili sauce, barbecue sauce, chutney, pickles, pickled vegetables, chocolate, vanilla, baked goods and pastries, pudding, ice cream, chewing gum, and candy.

Egg Anaphylaxis, swelling, sometimes flatulence and vomiting An allergic individual may not own any reaction to consuming food only prepared with yolk and not glair, or vice versa.
Fish Respiratory reactions, Anaphylaxis, oral allergy syndrome, sometimes vomiting One of three allergies to seafood, not to be conflated with allergies to crustaceans and mollusks.[1] Fish allergy sufferers own a 50% likelihood of being cross reactive with another fish species,[2] but some individuals are only allergic to one species, such as; tilapia,[3] salmon, [1] or cod.

A proper diagnosis is considered complicated due to these cross reactivity between fish species and other seafood allergies. [4] Hazard extends to exposure to cooking vapors or handling.

Fruit Mild itching, rash, generalized urticaria, oral allergy syndrome, abdominal pain, vomiting, anaphylaxis Mango, strawberries, banana, [5]avocado, and kiwi are common problems.[6] Severe allergies to tomatoes own also been reported. [7][8]
Garlic Dermatitis, asymmetrical pattern of fissure, thickening/shedding of the outer skin layers,[9]anaphylaxis
Hot peppers Skin rash, hives, throat tightness, tongue swelling, possible vomiting
Oats Dermatitis, respiratory problems, anaphylaxis
Maize Hives, pallor, confusion, dizziness, stomach pain, swelling, vomiting, indigestion, diarrhea, cough, tightness in throat, wheezing, shortness of breath, anaphylaxis Often a hard allergy to manage due to the various food products which contain various forms of corn.

Milk[10] Skin rash, hives, vomiting, diarrhea, constipation, stomach pain, flatulence, nasal congestion, dermatitis, blisters, anaphylaxis Not to be confused with lactose intolerance.[11]
Peanut[12] Anaphylaxis and swelling, sometimes vomiting Includes some cold-pressed peanut oils. Distinct from tree nut allergy, as peanuts are legumes.
Poultry Meat[13] Hives, swelling of, or under the dermis, nausea, vomiting, diarrhea, severe oral allergy syndrome, shortness of breath, rarely anaphylactic shock Very rare allergies to chicken, turkey, squab, and sometimes more mildly to other avian meats.

Not to be confused with secondary reactions of bird-egg syndrome. The genuine allergy has no causal relationship with egg allergy, nor is there any shut association with red meat allergy. Prevalence still unknown as of [14]

Red Meat[15] Hives, swelling,[16] dermatitis, stomach pain, nausea, vomiting, dizziness, fainting, shortness of breath,[17], rarely anaphylaxis Allergies to the sugar carbohydrate found in beef, venison, lamb, and pork called alpha-gal.

It is brought on by tick bites.[18][19] Allergic reaction to pork is an exception, as it may also be caused by pork-cat syndrome instead of alpha-gal allergy.

Rice Sneezing, runny nose, itching, stomachache, eczema. People with a rice allergy can be affected by eating rice or breathing in rice steam.
Sesame Possible respiratory, skin, and gastrointestinal reactions which can trigger serious systemic anaphylactic responses.[20][21] By law, foods containing sesame must be labeled so in European Union, Canada, Australia, and New Zealand.[20]
Shellfish Respiratory symptoms, Anaphylaxis, oral allergy syndrome, gastrointestinal symptoms, rhinitis, conjunctivitis Shellfish allergies are highly cross reactive, but its prevalence is generally higher than that of fish allergy.

As of six allergens own been identified to prawn alone; along with crab it‘s the major culprit of seafood anaphylaxis.[1] In reference to it as one of the “Big 8” [22] or “major 14” allergens it is sometimes specified as a “crustacean shellfish” allergy, or more simply, a “crustacean allergy”.[23][24] Sometimes it is conflated with an allergy to molluscan shellfish but finish tolerance to one but not the other isn’t unusual. Most generally, a mono-sensitive individual will experience a crustacean allergy alone with tolerance to mollusks, rather than vice versa.[1]

Soy Anaphylaxis, sometimes vomiting
Sulfites Hives, rash, redness of skin, headache (particular frontal), burning behind eyes, breathing difficulties (anaphylaxis) Used as a preserving agent in numerous diverse foods, such as raisins, dried peaches, various other dried fruit, canned or frozen fruits and vegetables, wines, vinegars and processed meats.

Tartrazine Skin irritation, hives, rash Synthetic yellow food coloring, also used for bright green coloring
Tree nut[25] Anaphylaxis, swelling, rash, hives, sometimes vomiting Hazard extends to exposure to cooking vapors, or handling. Distinct from peanut allergy, as peanuts are legumes.
Wheat[26] Eczema (atopic dermatitis), Hives, asthma, hay fever, angioedema, abdominal cramps, Celiac disease, diarrhea, temporary (3 or 4 day) mental incompetence, anemia, nausea, and vomiting[27] Not to be confused with Celiac Disease or NCGS (Non Celiac Gluten Sensitivity).

While wheat allergies are «true» allergies, Celiac Disease is an autoimmune disease.[28]

medical

Main article: Drug allergy

Name Possible reaction(s) Remarks
Balsam of Peru Redness, swelling, itching, allergiccontact dermatitis reactions, stomatitis (inflammation and soreness of the mouth or tongue), cheilitis (inflammation, rash, or painful erosion of the lips, oropharyngealmucosa, or angles of their mouth), pruritus, hand eczema, generalized or resistant plantardermatitis, rhinitis, conjunctivitis, and blisters.

Present in numerous drugs, such as hemorrhoid suppositories and ointment (e.g. Anusol), cough medicine/suppressant and lozenges, diaper rash ointments, oral and lip ointments, tincture of benzoin, wound spray (it has been reported to inhibit Mycobacterium tuberculosis as well as the common ulcer-causing bacteria H. pylori in test-tube studies), calamine lotion, surgical dressings, dental cement, eugenol used by dentists, some periodontal impression materials, and in the treatment of dry socket in dentistry.

Tetracycline Many, including: severe headache, dizziness, blurred vision, fever, chills, body aches, flu symptoms, severe blistering, peeling, dark colored urine[29][30][31]
Dilantin Many, including: swollen glands, simple bruising or bleeding, fever, sore throat[32][33][34]
Tegretol (carbamazepine) Shortness of breath, wheezing or difficulty breathing, swelling of the face, lips, tongue etc., hives[35][36][37]
Penicillin Diarrhea, hypersensitivity, nausea, rash, neurotoxicity, urticaria
Cephalosporins Maculopapular or morbilliform skin eruption, and less commonly urticaria, eosinophilia, serum-sickness–like reactions, and anaphylaxis.[38]
Sulfonamides Urinary tract disorders, haemopoietic disorders, porphyria and hypersensitivity reactions, Stevens–Johnson syndrometoxic epidermal necrolysis
Non-steroidal anti-inflammatories (cromolyn sodium, nedocromil sodium, etc.) Many, including: swollen eyes, lips, or tongue, difficulty swallowing, shortness of breath, rapid heart rate[39]
Intravenous contrast dye Anaphylactoid reactions and contrast-induced nephropathy
Local anesthetics Urticaria and rash, dyspnea, wheezing, flushing, cyanosis, tachycardia[40]

Environmental

Main article: Allergy §Other environmental factors

Name Possible reaction(s) Remarks
Balsam of Peru Redness, swelling, itching, allergiccontact dermatitis reactions, stomatitis (inflammation and soreness of the mouth or tongue), cheilitis (inflammation, rash, or painful erosion of the lips, oropharyngealmucosa, or angles of their mouth), pruritus, hand eczema, generalized or resistant plantardermatitis, rhinitis, conjunctivitis, and blisters.

A number of national and international surveys own identified Balsam of Peru as being in the «top five» allergens most commonly causing patch test reactions in people referred to dermatology clinics.[41][42]
Pollen Sneezing, body ache, headache (in rare cases, extremely painful cluster headaches may happen due to allergic sinusitis; these may leave a temporary time period of 1 and a half to 2 days with eye sensitivity), allergic conjunctivitis (includes watery, red, swelled, itchy, and irritating eyes), runny nose, irritation of the nose, nasal congestion, minor fatigue, chest pain and discomfort, coughing, sore throat, facial discomfort (feeling of stuffed face) due to allergic sinusitis, possible asthma attack, wheezing
Cat Sneezing, itchy swollen eyes, rash, congestion, wheezing
Dog Rash, sneezing, congestion, wheezing, vomiting from coughing, Sometimes itchy welts.

Caused by dander, saliva or urine of dogs, or by dust, pollen or other allergens that own been carried on the fur.[43] Allergy to dogs is present in as much as 10 percent of the population.[43]
Insect sting Hives, wheezing, possible anaphylaxis Possible from bee or wasp stings, or bites from mosquitoes or flies love Leptoconops torrens.
Mold Sneeze, coughing, itchy, discharge from the nose, respiratory irritation, congested feeling,[44] joint aches, headaches, fatigue[45]
Perfume Itchy eyes, runny nose, sore throat, headaches, muscle/joint pain, asthma attack, wheezing, chest pain, blisters
Cosmetics Contact dermatitis,[46] irritant contact dermatitis, inflammation, redness,[47] conjunctivitis[48] ,sneezing
Semen Burning, pain and swelling, possibly for days, swelling or blisters, vaginal redness,[49] fever, runny nose, extreme fatigue[50][51][52][53][54] In a case study in Switzerland, a lady who was allergic to Balsam of Peru was allergic to her boyfriend’s semen following intercourse, after he drank large amounts of Coca-Cola.[55]
Latex Contact dermatitis, hypersensitivity
Water (see note) Epidermal itching Strictly aquagenic pruritus or aquagenic urticaria, but freezing urticaria may also be described as a «water allergy,» in which water may cause hives and anaphylaxis
House dust mite[56] Asthma Home allergen reduction may be recommended
Nickel (nickel sulfate hexahydrate) Allergic contact dermatitis, dyshidrotic eczema[57][58]
Gold (gold sodium thiosulfate) Allergic contact dermatitis
Chromium Allergic contact dermatitis
Cobalt chloride Allergic contact dermatitis
Formaldehyde Allergic contact dermatitis
Photographic developers Allergic contact dermatitis
Fungicide Allergic contact dermatitis, fever, anaphylaxis

Contact

Many substances can cause an allergic reaction when in contact with the human integumentary system.


Further reading

1Department of Health, Human Performance and Recreation, Baylor University, Waco, Texas, USA

*Corresponding Author:Christie Maria Sayes, Environmental Science Department, Baylor University, One Bear Put , Waco, TX ;

Food allergy, Food sensitivity, Food intolerance, Environment, 10 Essential services

Results

Using this search strategy, we identified a entire of unique articles in English, while carefully eliminating any frequencies in search results among and between the search engines employed.

After other exclusion criteria were accounted for, 11 articles remained for review. The bibliographies of these 11 papers were also examined for additional relevant articles, but relevant cited articles were already captured in the initial analyses. These articles are limited to research studies with experimental designs and are summarized in Table 2. Our analysis is outlined as follows: first, brief overviews of Individual allergens, their prevalence and diagnoses; historical perspectives (Current era vs.

past eras), discussion of Allergy vs. intolerance/sensitivity, and Known causes and pre-existing health conditions are discussed. Second, the five working hypotheses in this field of study are explained. Third, the environmental factors contributing to the onset of food allergies are proposed.

Paper Reference

Brief Study Design

Environmental Factor
Measure

Human Health
Measure

Result

Gern et al.

[5]

Pet exposure in the home
compared against
cytokine secretion in infants

Dogs

Indicators of atopy

Having a dog in infancy is
associated with higher
cytokine secretion
profiles and reduced allergic
sensitization

Kilpelainen et al. [7]

Self-reported wheezing from
Finnish students
( yr.) collected via
questionnaire

Childhood farm
environment

Food allergy,
allergic
rhinitis and/or
allergic
conjunctivitis

The childhood farm
environment independently
reduced the risk for physician-
diagnosed allergies

Liu et al.

[8]

Sensitization measured by
skin prick on Chinese
twin pairs ( yr.)

Living conditions,
environment,

and genetics

Peanut and
shellfish food
sensitization

Sensitivity to common food
allergens is influenced
by genetic and
environmental f actors

Leynaert et al. [6]

Questionnaire on farm
exposure in childhood in
2 French centers

Childhood farm
environment &
D14 CT
polymorphism

Atopic
sensitization

CD14 CT and farm
childhood environment
exposure may
modify the development
of atopy

Simpson et al.

[9]

Population-based birth
cohort study

Endotoxin in
home dust

Allergic
sensitization
and eczema

Increasing endotoxin exposure
is associated
with reduced risk of
allergic sensitization

Melén et al. [3]

Birth cohort study

Air pollution from
local traffic

Allergic
disease and
inflammatory
response

Long term exposure to
traffic pollutions
can increase allergy
sensitization

Lawlis et al. [10]

Online survey of principals
on school allergy awareness

School environment

Food-induced
allergic
reactions
(i.e.

anaphylaxis)
from milk, eggs,
peanuts,& seafood

Detailed awareness and
management
guidelines are integral for
schools to adequately
manage foodinduced allergic
reactions, in the
school environment

Makhija
et al. [11]

Questionnaires on home
demographics of mothers
and fathers of food allergic
children

Home environment
and
demographic
characteristics

Eczema, atopic
diseases, & food
allergies

Parents of food allergic
children found
higher rates of sensitization to
foods and aeroallergens
compared with the
general population

Majowicz
et al.

[12]

Conceptual model

Built and natural
environment

Foodborne illness,
food insecurity,
obesity, & food
allergy

Health practitioners should
consider how targeted
public health actions produce
positive or negative population
health impacts

Ben- Shoshan
et al. [13]

Telephone survey of individuals
with probable self
reported food allergies

Personal/family
history of atopy,
sociodemographi cs,
& lifestyle habits

Food allergy (i.e.
milk, egg,
peanut, tree nut,
shellfish, fish,
wheat, soy,
or sesame)

Development of eczema in
the first 2 years of
life is consistently
associated with food allergies

Bedolla- Barajas
et al.

[14]

Questionnaire to parents of
children ( yr.)
needing allergy treatment

Demographic and
clinical
data history

Oral allergy
syndrome
(OAS)

OAS is not uncommon
in our
environment; pineapple was the
main food related .
Quercus sp. was the pollen
associated

Xu et al. [15]

Questionnaire to parents
of Chinese
children ( yr.)
with atopic dermatitis

Home environment

Atopic
dermatitis

Home renovation/ redecoration,
new furniture, indoor mold,
urban residency, heredity
disposition and
food allergy can be risk factors for
childhood allergy development

Table 2: Summary of the research articles from the peer-reviewed literature that relates an environmental factor to the onset of an allergic reaction, sensitization, or disease.

Human health outcomes

The long-term human health outcomes that could happen from food allergies include increased allergic reactions (to more than one allergen), chronic psychological effects, and decreased life expectancy.

It is common among people with one food allergy to develop additional allergies and those allergens result in an anaphylactic reaction [1, 4, 53]. For some food allergies, children own a high probability of outgrowing the allergic reaction by the time they grow to adulthood; however, a peanut or tree nut allergy, which own the highest rates of anaphylaxis, are rarely outgrown [2, 27, 54]. Food allergies can also affect quality of life and can even cause psychological distress []. Food allergies developed in adulthood can cause a significant adjustment, which has shown to be hard for people.

If a person has several food allergies, as well as asthma, s/he develop aversions to food, lack in socialization, and difficulty breathing [19, 59, 60]. Specifically, eliminating certain foods in the diet results in missing nutrients. Although rare, death can happen as a result of an allergic reaction [61]. This generally occurs in people who own anaphylactic reactions if treatment is not timely or if the reaction is not noticed. Public health policies from the 10 essential public health services provide a suitable framework to develop best practices for individuals, healthcare practitioners, charities, recreation organizations, schools, and community services to follow.

Public health systems (i.e. the network of every public, private, and voluntary entities in a community) deliver essential public health services. Briefly, the 10 essential services include monitoring health, diagnosing problems and identifying hazards, informing people, mobilizing partnerships, developing policies, enforcing regulations, linking people to services, assuring competencies in workforce, evaluating effectiveness, and researching innovative solutions [62].

Essential Service

Interface with Food Allergies and the Environment

1
Monitor Health

• Be aware of common allergies and incidence rates
• Assess the health status of their individuals

2
Diagnose and Investigate

• Identify and investigate health threats in a timely manner
• Create action plan to address emerging health related threats

3
Inform, Educate, Empower

• Prevent health emergencies through education
• Inform school communities through the use of signage

4
Mobilize Community Partnerships

• Establish relationships between the school, the community, the parents, and the local physicians
• Ensure roles and responsibilities in case of an emergency
• Form a local coalition to promote allergy friendly food establishments, schools, and other public places

5
Develop Policies

• Ban certain allergens from the location
• Protect the health of the most vulnerable populations

6
Enforce Laws

• Utilize and enforce food allergy regulations
• Provide alternative allergen-friendly food options

7
Link to Care

• Provide constant management and surveillance
• Hire practitioners who can diagnose and treat those with food allergies
• Provide safe spaces in schools for children with food allergies to go
• Provide grocery stores with allergy friendly food
• Provide allergy friendly and safe food establishments
• Ensure resources provided are affordable and available to every people regardless of race and/or culture

8
Guarantee Capable Workforce

• Employ practitioners that up to date on the most current research in the field of food allergies
• Educate healthcare workers, teachers, and food service handlers

9
Evaluate

• Ensure that the policies, professionals, and regulations in put are working
• Assess efficacy of policies
• Improve upon deficiencies

10
Research

• Continue to conduct research in the field of food allergies
• Engage efforts for diagnosis, treatment, and cures
• Seek prevention strategies and analyze costs versus benefits

Table 3: The 10 essential services as they relate to food allergy occurrences.
Table 3 lists the 10 essential services and explains how each relates to food allergy occurrences.

Currently, the following components provide athletic services towards addressing the food allergy epidemic, as it relates to environmental factors, in the United States:

  • Policies are developed. Certain allergens are banned from specific locations and the most vulnerable populations are protected.
  • Workforce is capable. Continuing educations is available for practitioners, healthcare workers, teachers, and food service handlers.
  • Community partnerships are mobilized.

    Relationships between schools, the community centers, affected individuals (or parents of individuals), food establishments, and local physicians are established and the roles and responsibilities of each stakeholder are defined.

  • Link to Healthcare is known. Practitioners who can diagnose and treat those with food allergies are trained, hired, and supplied with resources.
  • Health is monitored. Healthcare practitioners are aware of common allergies and incidence rates in localities and assess the health status of individuals.
  • Regulations are enforced.

    Alternative allergen-friendly food options are available.

  • The system is evaluated. Policies and regulations are in put and working.

Conversely, a few challenges and data gaps in the field of environmental factors and their contribution to the food allergy epidemic still exist. The following components of the 10 essential services currently provide insufficient resources towards addressing the food allergy epidemic, as it relates to environmental factors, in the United States:

Conversely, a few challenges and data gaps in the field of environmental factors and their contribution to the food allergy epidemic still exist.

The following components of the 10 essential services currently provide insufficient resources towards addressing the food allergy epidemic, as it relates to environmental factors, in the United States:

  • Research: Several studies contain contradicting information. Ethnicity plays a role in the risk of some individuals developing a food allergy; however, the conclusions are not uniform across every studies and no trends own been founds. Because of this, it is increasingly hard to establish causation for food allergy development.
  • Prevention: There is a lack of information (i.e. protocols, guidance documents, or educational material) available for individuals to prevent exacerbation of existing allergies or development of new allergies.
  • Diagnosis: Due to the increased prevalence of individuals self-diagnosing, precise incidence rates are outdated and lack correlations with environmental health, urbanization, food system and accessibility, geography, socioeconomic, or other demographic data.

Recent research efforts own found more success in correlating environment factors and food allergies when more than one variable, such as environmental health, urbanization, food system and accessibility, geography, socioeconomic, or other demographic data.

Dempfle et al. [63] suggests that by looking at both genetic and environmental factors together, more conclusive results can be obtained [63]. Simpson et al hypothesizes that precision medicine (a.k.a. personalized medications) is a possible intervention for food and seasonal allergies [9]. Through the use of precision medication, allergens can be directly targeted and unintended drug-induced side effects may be prevented.

The five working hypotheses postulating the sources of food allergies deserve further investigations and possible interventions. In any intervention regarding food allergies, starting young and early exposure is key. Any of the possible interventions such as dermal or oral introduction are most affective if done early on in life.

Recommendations for further research include identifying potential combinations of gene, introducing food exposure in early life stage and through a variety of exposure routes, and developing frameworks for designing precision medicines.

The food allergy hypotheses

Through the review of the scientific literature, several hypotheses were presented, tested, and either proven true or inconclusive. These hypotheses purpose to explain some of possible reasons behind the current allergy epidemic and offer recommendations to prevent allergies from developing in otherwise healthy individuals.

These five (5) hypotheses include:

Recent research efforts own found more success in correlating environment factors and food allergies when more than one variable, such as environmental health, urbanization, food system and accessibility, geography, socioeconomic, or other demographic data. Dempfle et al. [63] suggests that by looking at both genetic and environmental factors together, more conclusive results can be obtained [63]. Simpson et al hypothesizes that precision medicine (a.k.a. personalized medications) is a possible intervention for food and seasonal allergies [9].

Through the use of precision medication, allergens can be directly targeted and unintended drug-induced side effects may be prevented.

The five working hypotheses postulating the sources of food allergies deserve further investigations and possible interventions. In any intervention regarding food allergies, starting young and early exposure is key. Any of the possible interventions such as dermal or oral introduction are most affective if done early on in life. Recommendations for further research include identifying potential combinations of gene, introducing food exposure in early life stage and through a variety of exposure routes, and developing frameworks for designing precision medicines.

The food allergy hypotheses

Through the review of the scientific literature, several hypotheses were presented, tested, and either proven true or inconclusive.

These hypotheses purpose to explain some of possible reasons behind the current allergy epidemic and offer recommendations to prevent allergies from developing in otherwise healthy individuals. These five (5) hypotheses include:

  • Antioxidant production hypothesis
  • Hygiene hypothesis
  • Dietary fat intake hypothesis
  • Vitamin D exposure hypothesis
  • Dual-allergen exposure hypothesis

Dietary fat intake hypothesis (H1): The dietary fat intake hypothesis offers the thought that reduction in consumption of animal fats and increase in margarine and vegetable oils use has led to the decrease in common food allergies [4, 36].

Individuals use margarine and vegetable oil in their diets in an increasing rate due to the conception that these oils are a healthier alternative to animal fats. Some literature presents a possible correlation in a decrease in animal fats and a positive correlation with an increase in food allergies [4]. Through literature search, papers were found to pertain to this hypothesis (Figure 3).

Antioxidant production hypothesis (H2): The antioxidant hypothesis argues that the decrease in consumption of unused fruit and vegetables accounts for food allergies and the adverse outcome of asthma [4, 37].

Fruits and vegetables contain vital nutrients and antioxidants. These nutrients and antioxidants frolic significant roles in maintaining health and fighting infection. With decreased fruit and vegetable intake, individuals do not get necessary essential elements needed for building sufficient immune system. Through a search of the literature, articles included the antioxidant hypothesis (Figure 3).

Vitamin D exposure hypothesis (H3): The vitamin D hypothesis has been postulated in two diverse (i.e.

opposing) forms. The first form argues that increases of vitamin D levels own led to increased food allergies; while the second form argues that decreases of vitamin D levels own led to increased food allergies [4, 38]. The first form argues that because of an increased consumption of Vitamin D from sources such as dairy products, more children experience an increase in food allergies [39]. The second form presents the thought that a lack of Vitamin D, mainly in the form of sunlight, leads to an increased risk of food allergies [40].

Several studies own been conducted comparing epinephrine injection (a.k.a. EpiPen®) usage rates in northern United States to southern United States []. States in the northern region had higher rates of food allergies as well as less exposure to sunlight. The Vitamin D exposure hypothesis has been frequently evaluated. A literature search revealed 80 papers on the topic (Figure 3).

Hygiene hypothesis (H4): Studies testing the hygiene hypothesis own rarely focused on food allergies, as the adverse outcome, alone. However, the hypothesis examines the role of commensal gut flora in the development of food allergies [4, 45, 46].

Studies focused on the effects of protecting children from microorganism exposure and the chances of food allergy development [47]. Exposing children to microorganisms has been shown to strengthen the immune system [48, 49]. The hygiene hypothesis is the most commonly studied food allergy hypothesis. A review of the literature presented papers on the topic (Figure 3). This also was the most researched hypothesis through clinical experiments presenting with quantitative findings.

Dual-allergen exposure hypothesis (H5): The final food allergy hypothesis involves dual- allergen exposure and argues that if a food allergy only occurs if the allergen is presented to an individual [4, 50, 51].

More specifically, if a certain food is not exposed to a culture or community, there should be no risk of developing an allergy to that food item. This was evident in Northern Europe in the ’s [52]. The dual-allergen exposure hypothesis is the least researched hypothesis. A literature search presented only 10 papers on the topic (Figure 3). The papers that were found every consisted of review articles. This hypothesis has a lot of room for growth and research.

Methods

We performed a structured literature search focused on identifying every relevant human studies related to environmental factors and food allergies. Multiple databases were queried between November and May PubMed, Scopus, and Web of Science search engines were utilized with keyword searches.

Papers were included if they were tagged with at least one search term from Group A and the term “environment*” from Group term B (Table 1). Further literature research narrowed the field to pediatric relevance. The most common themes identified from the original Group B term included: environmental factors, farm environment, smoking, and air pollution. Resultant papers written in English, found in the keyword search, and peer-reviewed were included in the analysis.

Searches included both research and review articles on humans, but excluded articles using animal or cell-based models. Other inclusion criteria include specific environmental factors noted in abstract and cohorts of children or young adults.

Databases

Group A terms

Group B terms

Number of papers returned

PubMed

food allergy

environment*

food sensitivity

1

food intolerance

9

Scopus

food allergy

environment*

food sensitivity

4

food intolerance

23

Web of Science

food allergy

environment*

food sensitivity

1

food intolerance

10

Table 1: Search terms for literature review.

*indicates end-truncated search term. Terms entered into database with quotation marks returned results with exact matches. Data includes both research and review articles.

Acknowledgments

The authors thank Baylor University for financial support.

Conclusion

In conclusion, food allergies are a field that more research needs to be done in. A lot of studies done own found correlations but own failed to prove causation. It is known that asthma can increase the risk of developing food allergies. There is also evidence supporting the environment playing a role but to what extent is still unknown and still being studied. Without causations and known ways to prevent food allergies, the epidemic will continue to grow and continue to affect millions of people.

Human health outcomes

The long-term human health outcomes that could happen from food allergies include increased allergic reactions (to more than one allergen), chronic psychological effects, and decreased life expectancy.

It is common among people with one food allergy to develop additional allergies and those allergens result in an anaphylactic reaction [1, 4, 53]. For some food allergies, children own a high probability of outgrowing the allergic reaction by the time they grow to adulthood; however, a peanut or tree nut allergy, which own the highest rates of anaphylaxis, are rarely outgrown [2, 27, 54]. Food allergies can also affect quality of life and can even cause psychological distress [].

Food allergies developed in adulthood can cause a significant adjustment, which has shown to be hard for people. If a person has several food allergies, as well as asthma, s/he develop aversions to food, lack in socialization, and difficulty breathing [19, 59, 60]. Specifically, eliminating certain foods in the diet results in missing nutrients. Although rare, death can happen as a result of an allergic reaction [61]. This generally occurs in people who own anaphylactic reactions if treatment is not timely or if the reaction is not noticed. Public health policies from the 10 essential public health services provide a suitable framework to develop best practices for individuals, healthcare practitioners, charities, recreation organizations, schools, and community services to follow.

Public health systems (i.e. the network of every public, private, and voluntary entities in a community) deliver essential public health services. Briefly, the 10 essential services include monitoring health, diagnosing problems and identifying hazards, informing people, mobilizing partnerships, developing policies, enforcing regulations, linking people to services, assuring competencies in workforce, evaluating effectiveness, and researching innovative solutions [62].

Essential Service

Interface with Food Allergies and the Environment

1
Monitor Health

• Be aware of common allergies and incidence rates
• Assess the health status of their individuals

2
Diagnose and Investigate

• Identify and investigate health threats in a timely manner
• Create action plan to address emerging health related threats

3
Inform, Educate, Empower

• Prevent health emergencies through education
• Inform school communities through the use of signage

4
Mobilize Community Partnerships

• Establish relationships between the school, the community, the parents, and the local physicians
• Ensure roles and responsibilities in case of an emergency
• Form a local coalition to promote allergy friendly food establishments, schools, and other public places

5
Develop Policies

• Ban certain allergens from the location
• Protect the health of the most vulnerable populations

6
Enforce Laws

• Utilize and enforce food allergy regulations
• Provide alternative allergen-friendly food options

7
Link to Care

• Provide constant management and surveillance
• Hire practitioners who can diagnose and treat those with food allergies
• Provide safe spaces in schools for children with food allergies to go
• Provide grocery stores with allergy friendly food
• Provide allergy friendly and safe food establishments
• Ensure resources provided are affordable and available to every people regardless of race and/or culture

8
Guarantee Capable Workforce

• Employ practitioners that up to date on the most current research in the field of food allergies
• Educate healthcare workers, teachers, and food service handlers

9
Evaluate

• Ensure that the policies, professionals, and regulations in put are working
• Assess efficacy of policies
• Improve upon deficiencies

10
Research

• Continue to conduct research in the field of food allergies
• Engage efforts for diagnosis, treatment, and cures
• Seek prevention strategies and analyze costs versus benefits

Table 3: The 10 essential services as they relate to food allergy occurrences.
Table 3 lists the 10 essential services and explains how each relates to food allergy occurrences.

Currently, the following components provide athletic services towards addressing the food allergy epidemic, as it relates to environmental factors, in the United States:

Dietary fat intake hypothesis (H1): The dietary fat intake hypothesis offers the thought that reduction in consumption of animal fats and increase in margarine and vegetable oils use has led to the decrease in common food allergies [4, 36]. Individuals use margarine and vegetable oil in their diets in an increasing rate due to the conception that these oils are a healthier alternative to animal fats. Some literature presents a possible correlation in a decrease in animal fats and a positive correlation with an increase in food allergies [4].

Through literature search, papers were found to pertain to this hypothesis (Figure 3).

Antioxidant production hypothesis (H2): The antioxidant hypothesis argues that the decrease in consumption of unused fruit and vegetables accounts for food allergies and the adverse outcome of asthma [4, 37]. Fruits and vegetables contain vital nutrients and antioxidants. These nutrients and antioxidants frolic significant roles in maintaining health and fighting infection. With decreased fruit and vegetable intake, individuals do not get necessary essential elements needed for building sufficient immune system.

Through a search of the literature, articles included the antioxidant hypothesis (Figure 3).

Vitamin D exposure hypothesis (H3): The vitamin D hypothesis has been postulated in two diverse (i.e. opposing) forms. The first form argues that increases of vitamin D levels own led to increased food allergies; while the second form argues that decreases of vitamin D levels own led to increased food allergies [4, 38]. The first form argues that because of an increased consumption of Vitamin D from sources such as dairy products, more children experience an increase in food allergies [39].

The second form presents the thought that a lack of Vitamin D, mainly in the form of sunlight, leads to an increased risk of food allergies [40]. Several studies own been conducted comparing epinephrine injection (a.k.a. EpiPen®) usage rates in northern United States to southern United States []. States in the northern region had higher rates of food allergies as well as less exposure to sunlight. The Vitamin D exposure hypothesis has been frequently evaluated. A literature search revealed 80 papers on the topic (Figure 3).

Hygiene hypothesis (H4): Studies testing the hygiene hypothesis own rarely focused on food allergies, as the adverse outcome, alone.

However, the hypothesis examines the role of commensal gut flora in the development of food allergies [4, 45, 46]. Studies focused on the effects of protecting children from microorganism exposure and the chances of food allergy development [47]. Exposing children to microorganisms has been shown to strengthen the immune system [48, 49]. The hygiene hypothesis is the most commonly studied food allergy hypothesis. A review of the literature presented papers on the topic (Figure 3). This also was the most researched hypothesis through clinical experiments presenting with quantitative findings.

Dual-allergen exposure hypothesis (H5): The final food allergy hypothesis involves dual- allergen exposure and argues that if a food allergy only occurs if the allergen is presented to an individual [4, 50, 51]. More specifically, if a certain food is not exposed to a culture or community, there should be no risk of developing an allergy to that food item. This was evident in Northern Europe in the ’s [52]. The dual-allergen exposure hypothesis is the least researched hypothesis.

A literature search presented only 10 papers on the topic (Figure 3). The papers that were found every consisted of review articles. This hypothesis has a lot of room for growth and research.

Methods

We performed a structured literature search focused on identifying every relevant human studies related to environmental factors and food allergies. Multiple databases were queried between November and May PubMed, Scopus, and Web of Science search engines were utilized with keyword searches. Papers were included if they were tagged with at least one search term from Group A and the term “environment*” from Group term B (Table 1).

Further literature research narrowed the field to pediatric relevance. The most common themes identified from the original Group B term included: environmental factors, farm environment, smoking, and air pollution. Resultant papers written in English, found in the keyword search, and peer-reviewed were included in the analysis. Searches included both research and review articles on humans, but excluded articles using animal or cell-based models. Other inclusion criteria include specific environmental factors noted in abstract and cohorts of children or young adults.

Databases

Group A terms

Group B terms

Number of papers returned

PubMed

food allergy

environment*

food sensitivity

1

food intolerance

9

Scopus

food allergy

environment*

food sensitivity

4

food intolerance

23

Web of Science

food allergy

environment*

food sensitivity

1

food intolerance

10

Table 1: Search terms for literature review.

*indicates end-truncated search term. Terms entered into database with quotation marks returned results with exact matches. Data includes both research and review articles.

Acknowledgments

The authors thank Baylor University for financial support.

Conclusion

In conclusion, food allergies are a field that more research needs to be done in. A lot of studies done own found correlations but own failed to prove causation. It is known that asthma can increase the risk of developing food allergies.

There is also evidence supporting the environment playing a role but to what extent is still unknown and still being studied.

What is the most common food allergy in uk

Without causations and known ways to prevent food allergies, the epidemic will continue to grow and continue to affect millions of people.

Human health outcomes

The long-term human health outcomes that could happen from food allergies include increased allergic reactions (to more than one allergen), chronic psychological effects, and decreased life expectancy. It is common among people with one food allergy to develop additional allergies and those allergens result in an anaphylactic reaction [1, 4, 53]. For some food allergies, children own a high probability of outgrowing the allergic reaction by the time they grow to adulthood; however, a peanut or tree nut allergy, which own the highest rates of anaphylaxis, are rarely outgrown [2, 27, 54].

Food allergies can also affect quality of life and can even cause psychological distress []. Food allergies developed in adulthood can cause a significant adjustment, which has shown to be hard for people. If a person has several food allergies, as well as asthma, s/he develop aversions to food, lack in socialization, and difficulty breathing [19, 59, 60]. Specifically, eliminating certain foods in the diet results in missing nutrients. Although rare, death can happen as a result of an allergic reaction [61]. This generally occurs in people who own anaphylactic reactions if treatment is not timely or if the reaction is not noticed. Public health policies from the 10 essential public health services provide a suitable framework to develop best practices for individuals, healthcare practitioners, charities, recreation organizations, schools, and community services to follow.

Public health systems (i.e. the network of every public, private, and voluntary entities in a community) deliver essential public health services. Briefly, the 10 essential services include monitoring health, diagnosing problems and identifying hazards, informing people, mobilizing partnerships, developing policies, enforcing regulations, linking people to services, assuring competencies in workforce, evaluating effectiveness, and researching innovative solutions [62].

Essential Service

Interface with Food Allergies and the Environment

1
Monitor Health

• Be aware of common allergies and incidence rates
• Assess the health status of their individuals

2
Diagnose and Investigate

• Identify and investigate health threats in a timely manner
• Create action plan to address emerging health related threats

3
Inform, Educate, Empower

• Prevent health emergencies through education
• Inform school communities through the use of signage

4
Mobilize Community Partnerships

• Establish relationships between the school, the community, the parents, and the local physicians
• Ensure roles and responsibilities in case of an emergency
• Form a local coalition to promote allergy friendly food establishments, schools, and other public places

5
Develop Policies

• Ban certain allergens from the location
• Protect the health of the most vulnerable populations

6
Enforce Laws

• Utilize and enforce food allergy regulations
• Provide alternative allergen-friendly food options

7
Link to Care

• Provide constant management and surveillance
• Hire practitioners who can diagnose and treat those with food allergies
• Provide safe spaces in schools for children with food allergies to go
• Provide grocery stores with allergy friendly food
• Provide allergy friendly and safe food establishments
• Ensure resources provided are affordable and available to every people regardless of race and/or culture

8
Guarantee Capable Workforce

• Employ practitioners that up to date on the most current research in the field of food allergies
• Educate healthcare workers, teachers, and food service handlers

9
Evaluate

• Ensure that the policies, professionals, and regulations in put are working
• Assess efficacy of policies
• Improve upon deficiencies

10
Research

• Continue to conduct research in the field of food allergies
• Engage efforts for diagnosis, treatment, and cures
• Seek prevention strategies and analyze costs versus benefits

Table 3: The 10 essential services as they relate to food allergy occurrences.
Table 3 lists the 10 essential services and explains how each relates to food allergy occurrences.

Currently, the following components provide athletic services towards addressing the food allergy epidemic, as it relates to environmental factors, in the United States:

  • Policies are developed. Certain allergens are banned from specific locations and the most vulnerable populations are protected.
  • Workforce is capable. Continuing educations is available for practitioners, healthcare workers, teachers, and food service handlers.
  • Community partnerships are mobilized.

    Relationships between schools, the community centers, affected individuals (or parents of individuals), food establishments, and local physicians are established and the roles and responsibilities of each stakeholder are defined.

  • Link to Healthcare is known. Practitioners who can diagnose and treat those with food allergies are trained, hired, and supplied with resources.
  • Health is monitored. Healthcare practitioners are aware of common allergies and incidence rates in localities and assess the health status of individuals.
  • Regulations are enforced.

    Alternative allergen-friendly food options are available.

  • The system is evaluated. Policies and regulations are in put and working.

Conversely, a few challenges and data gaps in the field of environmental factors and their contribution to the food allergy epidemic still exist. The following components of the 10 essential services currently provide insufficient resources towards addressing the food allergy epidemic, as it relates to environmental factors, in the United States:

Conversely, a few challenges and data gaps in the field of environmental factors and their contribution to the food allergy epidemic still exist.

The following components of the 10 essential services currently provide insufficient resources towards addressing the food allergy epidemic, as it relates to environmental factors, in the United States:

  • Research: Several studies contain contradicting information. Ethnicity plays a role in the risk of some individuals developing a food allergy; however, the conclusions are not uniform across every studies and no trends own been founds. Because of this, it is increasingly hard to establish causation for food allergy development.
  • Prevention: There is a lack of information (i.e.

    protocols, guidance documents, or educational material) available for individuals to prevent exacerbation of existing allergies or development of new allergies.

  • Diagnosis: Due to the increased prevalence of individuals self-diagnosing, precise incidence rates are outdated and lack correlations with environmental health, urbanization, food system and accessibility, geography, socioeconomic, or other demographic data.

Recent research efforts own found more success in correlating environment factors and food allergies when more than one variable, such as environmental health, urbanization, food system and accessibility, geography, socioeconomic, or other demographic data.

Dempfle et al. [63] suggests that by looking at both genetic and environmental factors together, more conclusive results can be obtained [63]. Simpson et al hypothesizes that precision medicine (a.k.a. personalized medications) is a possible intervention for food and seasonal allergies [9]. Through the use of precision medication, allergens can be directly targeted and unintended drug-induced side effects may be prevented.

The five working hypotheses postulating the sources of food allergies deserve further investigations and possible interventions.

In any intervention regarding food allergies, starting young and early exposure is key. Any of the possible interventions such as dermal or oral introduction are most affective if done early on in life. Recommendations for further research include identifying potential combinations of gene, introducing food exposure in early life stage and through a variety of exposure routes, and developing frameworks for designing precision medicines.

Conclusion

In conclusion, food allergies are a field that more research needs to be done in. A lot of studies done own found correlations but own failed to prove causation.

It is known that asthma can increase the risk of developing food allergies. There is also evidence supporting the environment playing a role but to what extent is still unknown and still being studied. Without causations and known ways to prevent food allergies, the epidemic will continue to grow and continue to affect millions of people.

The food allergy hypotheses

Through the review of the scientific literature, several hypotheses were presented, tested, and either proven true or inconclusive.

These hypotheses purpose to explain some of possible reasons behind the current allergy epidemic and offer recommendations to prevent allergies from developing in otherwise healthy individuals. These five (5) hypotheses include:

Recent research efforts own found more success in correlating environment factors and food allergies when more than one variable, such as environmental health, urbanization, food system and accessibility, geography, socioeconomic, or other demographic data. Dempfle et al. [63] suggests that by looking at both genetic and environmental factors together, more conclusive results can be obtained [63].

Simpson et al hypothesizes that precision medicine (a.k.a. personalized medications) is a possible intervention for food and seasonal allergies [9]. Through the use of precision medication, allergens can be directly targeted and unintended drug-induced side effects may be prevented.

The five working hypotheses postulating the sources of food allergies deserve further investigations and possible interventions. In any intervention regarding food allergies, starting young and early exposure is key.

Any of the possible interventions such as dermal or oral introduction are most affective if done early on in life. Recommendations for further research include identifying potential combinations of gene, introducing food exposure in early life stage and through a variety of exposure routes, and developing frameworks for designing precision medicines.

Conclusion

In conclusion, food allergies are a field that more research needs to be done in.

A lot of studies done own found correlations but own failed to prove causation. It is known that asthma can increase the risk of developing food allergies. There is also evidence supporting the environment playing a role but to what extent is still unknown and still being studied. Without causations and known ways to prevent food allergies, the epidemic will continue to grow and continue to affect millions of people.

The food allergy hypotheses

Through the review of the scientific literature, several hypotheses were presented, tested, and either proven true or inconclusive.

These hypotheses purpose to explain some of possible reasons behind the current allergy epidemic and offer recommendations to prevent allergies from developing in otherwise healthy individuals. These five (5) hypotheses include:

  • Antioxidant production hypothesis
  • Hygiene hypothesis
  • Dietary fat intake hypothesis
  • Vitamin D exposure hypothesis
  • Dual-allergen exposure hypothesis

Dietary fat intake hypothesis (H1): The dietary fat intake hypothesis offers the thought that reduction in consumption of animal fats and increase in margarine and vegetable oils use has led to the decrease in common food allergies [4, 36].

Individuals use margarine and vegetable oil in their diets in an increasing rate due to the conception that these oils are a healthier alternative to animal fats. Some literature presents a possible correlation in a decrease in animal fats and a positive correlation with an increase in food allergies [4]. Through literature search, papers were found to pertain to this hypothesis (Figure 3).

Antioxidant production hypothesis (H2): The antioxidant hypothesis argues that the decrease in consumption of unused fruit and vegetables accounts for food allergies and the adverse outcome of asthma [4, 37].

Fruits and vegetables contain vital nutrients and antioxidants. These nutrients and antioxidants frolic significant roles in maintaining health and fighting infection. With decreased fruit and vegetable intake, individuals do not get necessary essential elements needed for building sufficient immune system. Through a search of the literature, articles included the antioxidant hypothesis (Figure 3).

Vitamin D exposure hypothesis (H3): The vitamin D hypothesis has been postulated in two diverse (i.e.

opposing) forms. The first form argues that increases of vitamin D levels own led to increased food allergies; while the second form argues that decreases of vitamin D levels own led to increased food allergies [4, 38]. The first form argues that because of an increased consumption of Vitamin D from sources such as dairy products, more children experience an increase in food allergies [39]. The second form presents the thought that a lack of Vitamin D, mainly in the form of sunlight, leads to an increased risk of food allergies [40].

Several studies own been conducted comparing epinephrine injection (a.k.a. EpiPen®) usage rates in northern United States to southern United States []. States in the northern region had higher rates of food allergies as well as less exposure to sunlight. The Vitamin D exposure hypothesis has been frequently evaluated. A literature search revealed 80 papers on the topic (Figure 3).

Hygiene hypothesis (H4): Studies testing the hygiene hypothesis own rarely focused on food allergies, as the adverse outcome, alone. However, the hypothesis examines the role of commensal gut flora in the development of food allergies [4, 45, 46].

Studies focused on the effects of protecting children from microorganism exposure and the chances of food allergy development [47]. Exposing children to microorganisms has been shown to strengthen the immune system [48, 49]. The hygiene hypothesis is the most commonly studied food allergy hypothesis. A review of the literature presented papers on the topic (Figure 3). This also was the most researched hypothesis through clinical experiments presenting with quantitative findings.

Dual-allergen exposure hypothesis (H5): The final food allergy hypothesis involves dual- allergen exposure and argues that if a food allergy only occurs if the allergen is presented to an individual [4, 50, 51].

More specifically, if a certain food is not exposed to a culture or community, there should be no risk of developing an allergy to that food item. This was evident in Northern Europe in the ’s [52]. The dual-allergen exposure hypothesis is the least researched hypothesis. A literature search presented only 10 papers on the topic (Figure 3). The papers that were found every consisted of review articles. This hypothesis has a lot of room for growth and research.

Acknowledgments

The authors thank Baylor University for financial support.

References

Dietary fat intake hypothesis (H1): The dietary fat intake hypothesis offers the thought that reduction in consumption of animal fats and increase in margarine and vegetable oils use has led to the decrease in common food allergies [4, 36].

Individuals use margarine and vegetable oil in their diets in an increasing rate due to the conception that these oils are a healthier alternative to animal fats. Some literature presents a possible correlation in a decrease in animal fats and a positive correlation with an increase in food allergies [4]. Through literature search, papers were found to pertain to this hypothesis (Figure 3).

Antioxidant production hypothesis (H2): The antioxidant hypothesis argues that the decrease in consumption of unused fruit and vegetables accounts for food allergies and the adverse outcome of asthma [4, 37].

Fruits and vegetables contain vital nutrients and antioxidants. These nutrients and antioxidants frolic significant roles in maintaining health and fighting infection. With decreased fruit and vegetable intake, individuals do not get necessary essential elements needed for building sufficient immune system. Through a search of the literature, articles included the antioxidant hypothesis (Figure 3).

Vitamin D exposure hypothesis (H3): The vitamin D hypothesis has been postulated in two diverse (i.e. opposing) forms. The first form argues that increases of vitamin D levels own led to increased food allergies; while the second form argues that decreases of vitamin D levels own led to increased food allergies [4, 38].

The first form argues that because of an increased consumption of Vitamin D from sources such as dairy products, more children experience an increase in food allergies [39]. The second form presents the thought that a lack of Vitamin D, mainly in the form of sunlight, leads to an increased risk of food allergies [40]. Several studies own been conducted comparing epinephrine injection (a.k.a. EpiPen®) usage rates in northern United States to southern United States []. States in the northern region had higher rates of food allergies as well as less exposure to sunlight.

The Vitamin D exposure hypothesis has been frequently evaluated. A literature search revealed 80 papers on the topic (Figure 3).

Hygiene hypothesis (H4): Studies testing the hygiene hypothesis own rarely focused on food allergies, as the adverse outcome, alone. However, the hypothesis examines the role of commensal gut flora in the development of food allergies [4, 45, 46]. Studies focused on the effects of protecting children from microorganism exposure and the chances of food allergy development [47]. Exposing children to microorganisms has been shown to strengthen the immune system [48, 49]. The hygiene hypothesis is the most commonly studied food allergy hypothesis.

A review of the literature presented papers on the topic (Figure 3). This also was the most researched hypothesis through clinical experiments presenting with quantitative findings.

Dual-allergen exposure hypothesis (H5): The final food allergy hypothesis involves dual- allergen exposure and argues that if a food allergy only occurs if the allergen is presented to an individual [4, 50, 51]. More specifically, if a certain food is not exposed to a culture or community, there should be no risk of developing an allergy to that food item. This was evident in Northern Europe in the ’s [52]. The dual-allergen exposure hypothesis is the least researched hypothesis.

A literature search presented only 10 papers on the topic (Figure 3). The papers that were found every consisted of review articles. This hypothesis has a lot of room for growth and research.

Acknowledgments

The authors thank Baylor University for financial support.

References

  • Teufel M, Biedermann T, Rapps N, et al. Psychological burden of food allergy. World Journal of Gastroenterology: WJG 13 ():
  • Amlot PL, Kemeny DM, Zachary C, Parkes P, Lessof MH.

    Oral allergy syndrome (OAS): symptoms of IgE-mediated hypersensitivity to foods. Clin Allergy. ;17(1)–CrossRef Scholar

  • Eggesbø M, Botten G, Stigum H, et al. Is delivery by cesarean section a risk factor for food allergy? Journal of Allergy and clinical Immunology ():
  • • Krogulska A, Dynowski J, Jedrzejczyk M, Sardecka I, Malachowska B, Wasowska-Krolikowska K. The impact of food allergens on airway responsiveness in schoolchildren with asthma: A a DBPCFC study.

    Pediatr Pulmonol. ;51(8)– This study shows that food allergens may enhance non-specific bronchial hyperresponsiveness.CrossRef Scholar

  • Ho MH-K, Wong WH-S, Chang C. Clinical spectrum of food allergies: A comprehensive review. Clinical reviews in allergy and immunology 46 ():
  • Yepes-Nunez JJ, Brozek JL, Fiocchi A, Pawankar R, Cuello-Garcia C, Zhang Y, et al. Vitamin D supplementation in primary allergy prevention: Systematic systematic review of randomized and non-randomized studies. Allergy. ;73(1)–CrossRef Scholar

  • Comstock SS, DeMera R, Vega LC, Boren EJ, Deane S, Haapanen LA, et al. Allergic reactions to peanuts, tree nuts, and seeds aboard commercial airliners.

    Ann Allergy Asthma Immunol. ;(1)–ef Scholar

  • Stefka AT, Feehley T, Tripathi P, et al. Commensal bacteria protect against food allergen sensitization. Proceedings of the National Academy of Sciences ():
  • Ziyab AH, Karmaus W, Zhang H, Holloway JW, Steck SE, Ewart S, et al. Allergic sensitization and filaggrin variants predispose to the comorbidity of eczema, asthma, and rhinitis: results from the Isle of Wight birth cohort. Clin Exp Allergy. ;44(9)–ef Scholar

  • Black PN, Sharpe S. Dietary fat and asthma: Is there a connection? European Respiratory Journal 10 ():
  • Heyman MB. Lactose intolerance in infants, children, and adolescents. Pediatrics ():
  • Tan THT, Ellis JA, Saffery R, et al.

    The role of genetics and environment in the rise of childhood food allergy. Clinical & Experimental Allergy 42 ():

  • Abo-Zaid G, Sharpe RA, Fleming LE, Depledge M, Osborne NJ. Association of baby eczema with childhood and adult asthma: analysis of data from the birth cohort study. Int J Environ Res Public Health. ;15(7).CrossRef Scholar

  • Cummings AJ, Knibb RC, King RM, et al.

    The psychosocial impact of food allergy and food hypersensitivity in children, adolescents and their families: A review. Allergy 65 ():

  • Sampson HA. Update on food allergy. Journal of Allergy and Clinical Immunology ():
  • •• Pettersson ME, Koppelman GH, Flokstra-de Blok BMJ, Kollen BJ, Dubois AEJ. Prediction of the severity of allergic reactions to foods. Allergy. ;73(7)– This study underwrites that the severity of double blind placebo controlled food challenges remains largely unpredictable.CrossRef Scholar

  • Du Toit G, Roberts G, Sayre PH, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy.

    New England Journal Medicine ():

  • Webber CM, England RW. Oral allergy syndrome: a clinical, diagnostic, and therapeutic challenge. Ann Allergy Asthma Immunol. ;(2)–8; quiz 9–10, CrossRef Scholar

  • Rhodes HL, Sporik R, Thomas P, Holgate ST, Cogswell JJ. Early life risk factors for adult asthma: a birth cohort study of subjects at risk. J Allergy Clin Immunol. ;(5)–ef Scholar

  • Hill DA, Grundmeier RW, Ram G, Spergel JM. The epidemiologic characteristics of healthcare provider-diagnosed eczema, asthma, allergic rhinitis, and food allergy in children: a retrospective cohort study. BMC Pediatr. ;CrossRef Scholar

  • Marklund B, Ahlstedt S, Nordström G.

    Health-related quality of life among adolescents with allergy-like conditions?with emphasis on food hypersensitivity. Health and Quality of Life Outcomes 2 ():

  • Kim JS, Nowak-W?grzyn A, Sicherer SH, et al. Dietary baked milk accelerates the resolution of cow’s milk allergy in children. Journal of Allergy and Clinical Immunology ():
  • Roberts G, Lack G. Relevance of inhalational exposure to food allergens. Curr Opin Allergy Clin Immunol. ;3(3)–ef Scholar

  • Dotterud CK, Storrø O, Johnsen R, et al. Probiotics in pregnant women to prevent allergic disease: A randomized, double-blind trial.

    British Journal of Dermatology ():

  • Melén E, Nyberg F, Lindgren CM, et al. Interactions between glutathione s-transferase p1, tumor necrosis factor, and traffic-related air pollution for development of childhood allergic disease. Environmental Health Perspectives ():
  • Flohr C, Perkin M, Logan K, Marrs T, Radulovic S, Campbell LE, et al. Atopic dermatitis and disease severity are the main risk factors for food sensitization in exclusively breastfed infants. J Invest Dermatol. ;(2)–CrossRef Scholar

  • Christie L, Hine RJ, Parker JG, et al.

    Food allergies in children affect nutrient intake and growth. Journal of the American Dietetic Association ():

  • Bock SA, Munoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. J Allergy Clin Immunol. ;(1)–ef Scholar

  • Hill DJ, Firer MA, Shelton MJ, Hosking CS. Manifestations of milk allergy in infancy: clinical and immunologic findings. J Pediatr. ;(2)–ef Scholar

  • Kramer MS, Matush L, Vanilovich I, Platt R, Bogdanovich N, Sevkovskaya Z, et al. Effect of prolonged and exclusive breast feeding on risk of allergy and asthma: cluster randomised trial.

    BMJ. ;()CrossRef Scholar

  • Roberts G, Golder N, Lack G. Bronchial challenges with aerosolized food in asthmatic, food-allergic children. Allergy. ;57(8)–ef Scholar

  • Simpson A, John SL, Jury F, et al. Endotoxin exposure, cd14, and allergic disease: An interaction between genes and the environment. American Journal of Respiratory and Critical Care Medicine ():
  • Murray CS, Canoy D, Buchan I, et al. Body mass index in young children and allergic disease: Gender differences in a longitudinal study.

    Clinical & Experimental Allergy 41 ():

  • Liu X, Zhang S, Tsai HJ, et al. Genetic and environmental contributions to allergen sensitization in a chinese twin study. Clinical & Experimental Allergy 39 ():
  • 7.

    Arabkhazaeli A, Vijverberg SJ, van Erp FC, Raaijmakers JA, van der Ent CK, van der Maitland Zee AH. Characteristics and severity of asthma in children with and without atopic conditions: a cross-sectional study. BMC Pediatr. ;CrossRef Scholar

  • James JM, Eigenmann PA, Eggleston PA, Sampson HA. Airway reactivity changes in asthmatic patients undergoing blinded food challenges.

    Am J Respir Crit Care Med. ;(2)–CrossRef Scholar

  • Camargo CA, Clark S, Kaplan MS, et al. Regional differences in epipen prescriptions in the United States: The potential role of vitamin d. Journal of Allergy and Clinical Immunology ():
  • Kim JS, Sinacore JM, Pongracic JA. Parental use of epipen for children with food allergies. Journal of Allergy and Clinical Immunology ():
  • Sicherer SH, Furlong TJ, Maes HH, Desnick RJ, Sampson HA, Gelb BD.

    Genetics of peanut allergy: a twin study. J Allergy Clin Immunol. ;(1 Pt 1)–ef Scholar

  • 8.

    Illi S, von Mutius E, Lau S, Nickel R, Niggemann B, Sommerfeld C, et al. The pattern of atopic sensitization is associated with the development of asthma in childhood. J Allergy Clin Immunol. ;(5)–CrossRef Scholar

  • Bedolla-Barajas M, Kestler-Gramajo A, Alcalá-Padilla G, et al. Prevalence of oral allergy syndrome in children with allergic diseases.

    Allergologia et Immunopathologia 45 ():

  • Jansen JJN, Kardinaal AFM, Huijbers G, et al. Prevalence of food allergy and intolerance in the adult dutch population. Journal of Allergy and Clinical Immunology 93 ():
  • Sicherer SH, Sampson HA. Food allergy. Journal of Allergy and Clinical Immunology (): SS
  • Farioli L, Losappio LM, Giuffrida MG, Pravettoni V, Micarelli G, Nichelatti M, et al. Mite-induced asthma and IgE levels to shrimp, mite, tropomyosin, arginine kinase, and Der p 10 are the most risk factors for challenge-provenshrimp allergy.

    Int Arch Allergy Immunol. ;(3–4)–CrossRef Scholar

  • •• Perkin MR, Logan K, Tseng A, Raji B, Ayis S, Peacock J, et al. Randomized trial of introduction of allergenic foods in breast-fed infants. N Engl J Med. ;(18)– This is a RCT in young children in which they show that early introduction of peanut and egg at the age of 3 months results in a reduction of peanut and egg allergy at a later age.CrossRef Scholar

  • Schroeder A, Kumar R, Pongracic JA, Sullivan CL, Caruso DM, Costello J, et al. Food allergy is associated with an increased risk of asthma. Clin Exp Allergy. ;39(2)–CrossRef Scholar

  • Koplin JJ, Osborne NJ, Wake M, Martin PE, Gurrin LC, Robinson MN, et al.

    Can early introduction of egg prevent egg allergy in infants? A population-based study. J Allergy Clin Immunol. ;(4)–CrossRef Scholar

  • Tariq SM, Matthews SM, Hakim EA, Arshad SH. Egg allergy in infancy predicts respiratory allergic disease by 4 years of age. Pediatr Allergy Immunol. ;11(3)–ef Scholar

  • Primeau MN, Kagan R, Joseph L, et al. The psychological burden of peanut allergy as perceived by adults with peanut allergy and the parents of peanut- allergic children. Clinical and Experimental Allergy 30 ():
  • Xu F, Yan S, Zheng Q, et al. Residential risk factors for atopic dermatitis in 3-to 6-year ancient children: A cross-sectional study in shanghai, china.

    International Journal of Environmental Research and Public Health ():

  • von Mutius E. The environmental predictors of allergic disease. Journal of Allergy and Clinical Immunology ():
  • Round JL, Mazmanian SK. The gut microbiota shapes intestinal immune responses during health and disease. Nature Reviews Immunology 9 ():
  • Ben-Shoshan M, Soller L, Harrington DW, et al. Eczema in early childhood, sociodemographic factors and lifestyle habits are associated with food allergy: A nested case-control study.

    International Archives of Allergy and Immunology ():

  • 1.

    Lai CK, Beasley R, Crane J, Foliaki S, Shah J, Weiland S, et al. Global variation in the prevalence and severity of asthma symptoms: phase three of the International Study of Asthma and Allergies in Childhood (ISAAC). Thorax. ;64(6)–CrossRef Scholar

  • Majowicz SE, Meyer SB, Kirkpatrick SI, et al. Food, health, and complexity: Towards a conceptual understanding to guide collaborative public health action. BMC Public Health 16 ():
  • Jackson KD, Howie LD, Akinbami LJ. Trends in allergic conditions among children: United states, (National Middle for Health Statistics Data Brief).National Middle for Health Statistics, Centers for Disease Control ().
  • Wjst M.

    Another explanation for the low allergy rate in the rural alpine foothills. Clinical and Molecular Allergy 3 (): 7.

  • Campbell CP, Yates DH. Lupin allergy: a hidden killer at home, a menace at work; occupational disease due to lupin allergy. Clin Exp Allergy. ;40(10)–CrossRef Scholar

  • Summers CW, Pumphrey RS, Woods CN, McDowell G, Pemberton PW, Arkwright PD. Factors predicting anaphylaxis to peanuts and tree nuts in patients referred to a specialist middle.

    J Allergy Clin Immunol. ;(3)–ef Scholar

  • Sicherer SH, Muñoz-Furlong A, Godbold JH, et al. Us prevalence of self-reported peanut, tree nut, and sesame allergy: year follow-up. Journal of Allergy and Clinical Immunology ():
  • Corso LC, Wiesner PJ, Halverson PK, et al. Using the essential services as a foundation for performance measurement and assessment of local public health systems. Journal of Public Health Management and Practice 6 ():
  • Leynaert B, Guilloud-Bataille M, Soussan D, et al. Association between farm exposure and atopy, according to the cd14 ct polymorphism.

    Journal of Allergy and Clinical Immunology ():

  • Scurlock AM, Burks AW, Jones SM. Oral immunotherapy for food allergy. Current Allergy and Asthma Reports 9 ():
  • •• Baur X. A compendium of causative agents of occupational asthma. J Occup Med Toxicol. ;8(1) A comprehensive overview of agents that may induce occupational asthma.CrossRef Scholar

  • Kemp AS. Epipen epidemic: Suggestions for rational prescribing in childhood food allergy. Journal of Paediatrics and Kid Health 39 ():
  • Makhija MM, Robison RG, Caruso D, et al.

    Patterns of allergen sensitization and self-reported allergic disease in parents of food allergic children. Annals of Allergy, Asthma & Immunology ():

  • Calvani M, Cardinale F, Martelli A, Muraro A, Pucci N, Savino F, et al. Risk factors for severe pediatric food anaphylaxis in Italy. Pediatr Allergy Immunol. ;22(8)–ef Scholar

  • Spergel JM, Paller AS. Atopic dermatitis and the atopic march. J Allergy Clin Immunol. ;(6 Suppl):S–CrossRef Scholar

  • Woods RK, Thien F, Raven J, Walters EH, Abramson M.

    Prevalence of food allergies in young adults and their relationship to asthma, nasal allergies, and eczema. Ann Allergy Asthma Immunol. ;88(2)–ef Scholar

  • Milner JD, Stein DM, McCarter R, et al. Early baby multivitamin supplementation is associated with increased risk for food allergy and asthma. Pediatrics ():
  • 2.

    Dahlman-Hoglund A, Renstrom A, Larsson PH, Elsayed S, Andersson E.

    Salmon allergen exposure, occupational asthma, and respiratory symptoms among salmon processing workers. Am J Ind Med. ;55(7)–CrossRef Scholar

  • Lack G. Epidemiologic risks for food allergy. Journal of Allergy and Clinical Immunology ():
  • Young E, Stoneham MD, Petruckevitch A, et al. A population study of food intolerance. The Lancet ():
  • Gern JE, Reardon CL, Hoffjan S, et al. Effects of dog ownership and genotype on immune development and atopy in infancy. Journal of Allergy and Clinical Immunology ():
  • 3.

    Rona RJ, Keil T, Summers C, Gislason D, Zuidmeer L, Sodergren E, et al.

    The prevalence of food allergy: a meta-analysis. J Allergy Clin Immunol. ;(3)–CrossRef Scholar

  • Marks GB, Mihrshahi S, Kemp AS, Tovey ER, Webb K, Almqvist C, et al. Prevention of asthma during the first 5 years of life: a randomized controlled trial. J Allergy Clin Immunol. ;(1)–CrossRef Scholar

  • Lack G, Fox D, Northstone K, et al. Factors associated with the development of peanut allergy in childhood. New England Journal of Medicine ():
  • Lack G. Epidemiologic risks for food allergy. J Allergy Clin Immunol.

    ;(6)–ef Scholar

  • 4.

    Savage J, Johns CB. Food allergy: epidemiology and natural history. Immunol Allergy Clin N Am. ;35(1)–CrossRef Scholar

  • Bager P, Wohlfahrt J, Westergaard T. Caesarean delivery and risk of atopy and allergic disesase: Meta-analyses. Clinical & Experimental Allergy 38 ():
  • Pumphrey RS, Roberts IS. Postmortem findings after fatal anaphylactic reactions. J Clin Pathol. ;53(4)–ef Scholar

  • 6.

    Liu AH, Jaramillo R, Sicherer SH, Wood RA, Bock SA, Burks AW, et al. National prevalence and risk factors for food allergy and relationship to asthma: results from the National Health and Nutrition Examination Survey – J Allergy Clin Immunol.

    ;(4)–CrossRef Scholar

  • Macpherson AJ, Harris NL. Interactions between commensal intestinal bacteria and the immune system. Nature Reviews Immunology 4 ():
  • Bergmann RL, Edenharter G, Bergmann KE, Forster J, Bauer CP, Wahn V, et al. Atopic dermatitis in early infancy predicts allergic airway disease at 5 years. Clin Exp Allergy. ;28(8)–CrossRef Scholar

  • Bock SA, Muñoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. Journal of Allergy and Clinical Immunology ():
  • Dempfle A, Scherag A, Hein R, et al.

    Gene? environment interactions for complicated traits: Definitions, methodological requirements and challenges. European Journal of Human Genetics 16 ():

  • van Ree R, Antonicelli L, Akkerdaas JH, Pajno GB, Barberio G, Corbetta L, et al. Asthma after consumption of snails in house-dust-mite-allergic patients: a case of IgE cross-reactivity. Allergy. ;51(6)–CrossRef Scholar

  • Guillet G, Guillet MH. Natural history of sensitizations in atopic dermatitis.

    A 3-year follow-up in children: food allergy and high risk of respiratory symptoms. Arch Dermatol. ;(2)–CrossRef Scholar

  • Tuft L, Blumstein G. Studies in food allergy — sensitization to unused fruits: clinical and experimental observations. J Allergy Ther. ;–ef Scholar

  • Sharief S, Jariwala S, Kumar J, et al. Vitamin d levels and food and environmental allergies in the united states: Results from the national health and nutrition examination survey Journal of Allergy and Clinical Immunology ():
  • 5.

    Venter C, Arshad SH. Epidemiology of food allergy. Pediatr Clin N Am. ;58(2)–CrossRef Scholar

  • Aziz I, Hadjivassiliou M, Sanders DS.

    The spectrum of noncoeliac gluten sensitivity. Nature Reviews Gastroenterology & Hepatology 12 ():

  • Mills ENC, Mackie AR, Burney P, et al. The prevalence, cost and basis of food allergy across europe. Allergy 62 ():
  • Panel NIoAaID-SE. Guidelines for the diagnosis and management of food allergy in the United States: Report of the niaid-sponsored expert panel. (Journal of Allergy and Clinical Immunology). National Institute of Allergy and Infectious Diseases.
  • Kilpelainen M, Terho EO, Helenius H, et al. Farm environment in childhood prevents the development of allergies.

    Clinical Experimental Allergy 30 ():

  • (FARE) FARE. Facts and statistics ().
  • Branum AM, Lukacs S. Food allergy among us children: Trends in prevalence and hospitalizations:US Department of Health and Human Services, Centers for Disease Control and Prevention, National Middle for Health Statistics ().
  • Misselwitz B, Pohl D, Frühauf H, et al. Lactose malabsorption and intolerance: Pathogenesis, diagnosis and treatment. United European Gastroenterology Journal 1 ():
  • •• Tsakok T, Marrs T, Mohsin M, Baron S, du Toit G, Till S, et al. Does atopic dermatitis cause food allergy?

    A systematic review. J Allergy Clin Immunol. ;(4)–8. This paper comprises a systematic analysis and review out of 66 research studies. It was concluded that there is a strong association between atopic dermatitis, food sensitization and food allergy.CrossRef Scholar

  • Irvine AD, McLean WH, Leung DY. Filaggrin mutations associated with skin and allergic diseases. N Engl J Med. ;(14)–CrossRef Scholar

  • Best KP, Sullivan TR, Palmer DJ, Gold M, Martin J, Kennedy D, et al.

    Prenatal omega-3 LCPUFA and symptoms of allergic disease and sensitization throughout early childhood — a longitudinal analysis of long-term follow-up of a randomized controlled trial. World Allergy Organ J. ;11(1)CrossRef Scholar

  • Ortolani C, Pastorello EA. Food allergies and food intolerances. Best Practice and Research Clinical Gastroenterology 20 ():
  • van Erp FC, Knulst AC, Kentie PA, Pasmans SG, van der Ent CK, Meijer Y. Can we predict severe reactions during peanut challenges in children?

    Pediatr Allergy Immunol. ;24(6)–CrossRef Scholar

  • Rona RJ, Keil T, Summers C, et al. The prevalence of food allergy: A meta-analysis. Journal of Allergy and Clinical Immunology ():
  • Meyer R, Fleming C, Dominguez-Ortega G, Lindley K, Michaelis L, Thapar N, et al. Manifestations of food protein induced gastrointestinal allergies presenting to a single tertiary paediatric gastroenterology unit. World Allergy Organ J. ;6(1)CrossRef Scholar

  • Allan K, Kelly FJ, Devereux G.

    Antioxidants and allergic disease: A case of too little or too much? Clinical and Experimental Allergy 40 ():

  • Weiss C, Muñoz-Furlong A, Furlong TJ, et al. Impact of food allergies on school nursing practice. The Journal of School Nursing 20 ():
  • Lawlis T, Bakonyi S, Williams LT. Food allergy in schools: The importance of government involvement. Nutrition and Dietetics ().
  • Sporik R, Hill DJ, Hosking CS. Specificity of allergen skin testing in predicting positive open food challenges to milk, egg and peanut in children.

    Clinical & Experimental Allergy 30 ():

  • Mansfield LE. Oral immunotherapy for peanut allergy in clinical practice is ready. In: Proceedings of the Allergy and Asthma Proceedings. OceanSide Publications, Inc 34 ():
  • Arshad SH, Tariq SM, Matthews S, et al. Sensitization to common allergens and its association with allergic disorders at age 4 years: A whole population birth cohort study. Pediatrics (): ee
  • Hourihane JO, Dean TP, Warner JO. Peanut allergy in relation to heredity, maternal diet, and other atopic diseases: results of a questionnaire survey, skin prick testing, and food challenges.

    BMJ. ;()–CrossRef Scholar

  • Bao Y, Chen Z, Liu E, Xiang L, Zhao D, Hong J. Risk factors in preschool children for predicting asthma during the preschool age and the early school age: a systematic review and meta-analysis. Curr Allergy Asthma Rep. ;17(12)CrossRef Scholar

  • Ortolani C, Ispano M, Pastorello E, Bigi A, Ansaloni R. The oral allergy syndrome. Ann Allergy. ;61(6 Pt 2)–PubMed Scholar

  • 9.

    Wang J, Visness CM, Sampson HA. Food allergen sensitization in inner-city children with asthma. J Allergy Clin Immunol. ;(5)–CrossRef Scholar

  • Salvatori N, Reccardini F, Convento M, Purinan A, Colle R, De Carli S, et al.

    Asthma induced by inhalation of flour in adults with food allergy to wheat. Clin Exp Allergy. ;38(8)–CrossRef Scholar

  • Gupta RS, Springston EE, Warrier MR, et al. The prevalence, severity, and distribution of childhood food allergy in the United States. Pediatrics:peds ():
  • Leser C, Hartmann AL, Praml G, Wuthrich B. The «“egg-egg»” syndrome: occupational respiratory allergy to airborne egg proteins with consecutive ingestive egg allergy in the bakery and confectionery industry.

    J Investig Allergol Clin Immunol. ;11(2)–PubMed

Figure 1: The progression of food allergy diagnosis. This figure shows the possible interactions a body can own to an allergen. The three stages are: no sensitivity to the food, food sensitivity, and food allergy.

Figure 2: Steps to overcome sensitivity related illness.

Figure 3: (A) Current hypothesized associations between food allergies and external factors and articles associated with them.

(B) Greatest number of papers published from search databases used versus the food allergy hypothesis number.

  • 1.

    Lai CK, Beasley R, Crane J, Foliaki S, Shah J, Weiland S, et al. Global variation in the prevalence and severity of asthma symptoms: phase three of the International Study of Asthma and Allergies in Childhood (ISAAC). Thorax. ;64(6)–CrossRef Scholar

  • 2.

    Dahlman-Hoglund A, Renstrom A, Larsson PH, Elsayed S, Andersson E. Salmon allergen exposure, occupational asthma, and respiratory symptoms among salmon processing workers.

    Am J Ind Med. ;55(7)–CrossRef Scholar

  • 3.

    Rona RJ, Keil T, Summers C, Gislason D, Zuidmeer L, Sodergren E, et al. The prevalence of food allergy: a meta-analysis. J Allergy Clin Immunol. ;(3)–CrossRef Scholar

  • 4.

    Savage J, Johns CB. Food allergy: epidemiology and natural history. Immunol Allergy Clin N Am. ;35(1)–CrossRef Scholar

  • 5.

    Venter C, Arshad SH. Epidemiology of food allergy. Pediatr Clin N Am. ;58(2)–CrossRef Scholar

  • 6.

    Liu AH, Jaramillo R, Sicherer SH, Wood RA, Bock SA, Burks AW, et al. National prevalence and risk factors for food allergy and relationship to asthma: results from the National Health and Nutrition Examination Survey – J Allergy Clin Immunol.

    ;(4)–CrossRef Scholar

  • 7.

    Arabkhazaeli A, Vijverberg SJ, van Erp FC, Raaijmakers JA, van der Ent CK, van der Maitland Zee AH. Characteristics and severity of asthma in children with and without atopic conditions: a cross-sectional study. BMC Pediatr. ;CrossRef Scholar

  • 8.

    Illi S, von Mutius E, Lau S, Nickel R, Niggemann B, Sommerfeld C, et al. The pattern of atopic sensitization is associated with the development of asthma in childhood. J Allergy Clin Immunol. ;(5)–CrossRef Scholar

  • 9.

    Wang J, Visness CM, Sampson HA. Food allergen sensitization in inner-city children with asthma. J Allergy Clin Immunol.

    ;(5)–CrossRef Scholar

  • Schroeder A, Kumar R, Pongracic JA, Sullivan CL, Caruso DM, Costello J, et al. Food allergy is associated with an increased risk of asthma. Clin Exp Allergy. ;39(2)–CrossRef Scholar

  • Hill DA, Grundmeier RW, Ram G, Spergel JM. The epidemiologic characteristics of healthcare provider-diagnosed eczema, asthma, allergic rhinitis, and food allergy in children: a retrospective cohort study. BMC Pediatr. ;CrossRef Scholar

  • Roberts G, Lack G. Relevance of inhalational exposure to food allergens.

    Curr Opin Allergy Clin Immunol. ;3(3)–ef Scholar

  • Tariq SM, Matthews SM, Hakim EA, Arshad SH. Egg allergy in infancy predicts respiratory allergic disease by 4 years of age. Pediatr Allergy Immunol. ;11(3)–ef Scholar

  • Spergel JM, Paller AS. Atopic dermatitis and the atopic march. J Allergy Clin Immunol. ;(6 Suppl):S–CrossRef Scholar

  • Rhodes HL, Sporik R, Thomas P, Holgate ST, Cogswell JJ. Early life risk factors for adult asthma: a birth cohort study of subjects at risk. J Allergy Clin Immunol. ;(5)–ef Scholar

  • Meyer R, Fleming C, Dominguez-Ortega G, Lindley K, Michaelis L, Thapar N, et al.

    Manifestations of food protein induced gastrointestinal allergies presenting to a single tertiary paediatric gastroenterology unit. World Allergy Organ J. ;6(1)CrossRef Scholar

  • •• Tsakok T, Marrs T, Mohsin M, Baron S, du Toit G, Till S, et al. Does atopic dermatitis cause food allergy? A systematic review. J Allergy Clin Immunol. ;(4)–8. This paper comprises a systematic analysis and review out of 66 research studies. It was concluded that there is a strong association between atopic dermatitis, food sensitization and food allergy.CrossRef Scholar

  • Flohr C, Perkin M, Logan K, Marrs T, Radulovic S, Campbell LE, et al.

    Atopic dermatitis and disease severity are the main risk factors for food sensitization in exclusively breastfed infants. J Invest Dermatol. ;(2)–CrossRef Scholar

  • Guillet G, Guillet MH. Natural history of sensitizations in atopic dermatitis. A 3-year follow-up in children: food allergy and high risk of respiratory symptoms. Arch Dermatol. ;(2)–CrossRef Scholar

  • Lack G. Epidemiologic risks for food allergy.

    J Allergy Clin Immunol. ;(6)–ef Scholar

  • Abo-Zaid G, Sharpe RA, Fleming LE, Depledge M, Osborne NJ. Association of baby eczema with childhood and adult asthma: analysis of data from the birth cohort study. Int J Environ Res Public Health. ;15(7).CrossRef Scholar

  • Bergmann RL, Edenharter G, Bergmann KE, Forster J, Bauer CP, Wahn V, et al. Atopic dermatitis in early infancy predicts allergic airway disease at 5 years. Clin Exp Allergy. ;28(8)–CrossRef Scholar

  • Bao Y, Chen Z, Liu E, Xiang L, Zhao D, Hong J. Risk factors in preschool children for predicting asthma during the preschool age and the early school age: a systematic review and meta-analysis.

    Curr Allergy Asthma Rep. ;17(12)CrossRef Scholar

  • Hourihane JO, Dean TP, Warner JO. Peanut allergy in relation to heredity, maternal diet, and other atopic diseases: results of a questionnaire survey, skin prick testing, and food challenges. BMJ. ;()–CrossRef Scholar

  • Sicherer SH, Furlong TJ, Maes HH, Desnick RJ, Sampson HA, Gelb BD. Genetics of peanut allergy: a twin study. J Allergy Clin Immunol. ;(1 Pt 1)–ef Scholar

  • Irvine AD, McLean WH, Leung DY. Filaggrin mutations associated with skin and allergic diseases. N Engl J Med. ;(14)–CrossRef Scholar

  • Ziyab AH, Karmaus W, Zhang H, Holloway JW, Steck SE, Ewart S, et al.

    Allergic sensitization and filaggrin variants predispose to the comorbidity of eczema, asthma, and rhinitis: results from the Isle of Wight birth cohort. Clin Exp Allergy. ;44(9)–ef Scholar

  • Marks GB, Mihrshahi S, Kemp AS, Tovey ER, Webb K, Almqvist C, et al. Prevention of asthma during the first 5 years of life: a randomized controlled trial. J Allergy Clin Immunol. ;(1)–CrossRef Scholar

  • Woods RK, Thien F, Raven J, Walters EH, Abramson M. Prevalence of food allergies in young adults and their relationship to asthma, nasal allergies, and eczema.

    Ann Allergy Asthma Immunol. ;88(2)–ef Scholar

  • Best KP, Sullivan TR, Palmer DJ, Gold M, Martin J, Kennedy D, et al. Prenatal omega-3 LCPUFA and symptoms of allergic disease and sensitization throughout early childhood — a longitudinal analysis of long-term follow-up of a randomized controlled trial. World Allergy Organ J. ;11(1)CrossRef Scholar

  • Yepes-Nunez JJ, Brozek JL, Fiocchi A, Pawankar R, Cuello-Garcia C, Zhang Y, et al.

    Vitamin D supplementation in primary allergy prevention: Systematic systematic review of randomized and non-randomized studies. Allergy. ;73(1)–CrossRef Scholar

  • Kramer MS, Matush L, Vanilovich I, Platt R, Bogdanovich N, Sevkovskaya Z, et al. Effect of prolonged and exclusive breast feeding on risk of allergy and asthma: cluster randomised trial. BMJ. ;()CrossRef Scholar

  • Koplin JJ, Osborne NJ, Wake M, Martin PE, Gurrin LC, Robinson MN, et al. Can early introduction of egg prevent egg allergy in infants?

    A population-based study. J Allergy Clin Immunol. ;(4)–CrossRef Scholar

  • •• Perkin MR, Logan K, Tseng A, Raji B, Ayis S, Peacock J, et al. Randomized trial of introduction of allergenic foods in breast-fed infants. N Engl J Med. ;(18)– This is a RCT in young children in which they show that early introduction of peanut and egg at the age of 3 months results in a reduction of peanut and egg allergy at a later age.CrossRef Scholar

  • Calvani M, Cardinale F, Martelli A, Muraro A, Pucci N, Savino F, et al.

    Risk factors for severe pediatric food anaphylaxis in Italy. Pediatr Allergy Immunol. ;22(8)–ef Scholar

  • Summers CW, Pumphrey RS, Woods CN, McDowell G, Pemberton PW, Arkwright PD. Factors predicting anaphylaxis to peanuts and tree nuts in patients referred to a specialist middle. J Allergy Clin Immunol. ;(3)–ef Scholar

  • Pumphrey RS, Roberts IS. Postmortem findings after fatal anaphylactic reactions. J Clin Pathol. ;53(4)–ef Scholar

  • van Erp FC, Knulst AC, Kentie PA, Pasmans SG, van der Ent CK, Meijer Y. Can we predict severe reactions during peanut challenges in children?

    Pediatr Allergy Immunol. ;24(6)–CrossRef Scholar

  • •• Pettersson ME, Koppelman GH, Flokstra-de Blok BMJ, Kollen BJ, Dubois AEJ. Prediction of the severity of allergic reactions to foods. Allergy. ;73(7)– This study underwrites that the severity of double blind placebo controlled food challenges remains largely unpredictable.CrossRef Scholar

  • Hill DJ, Firer MA, Shelton MJ, Hosking CS. Manifestations of milk allergy in infancy: clinical and immunologic findings.

    J Pediatr. ;(2)–ef Scholar

  • Bock SA, Munoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. J Allergy Clin Immunol. ;(1)–ef Scholar

  • James JM, Eigenmann PA, Eggleston PA, Sampson HA. Airway reactivity changes in asthmatic patients undergoing blinded food challenges. Am J Respir Crit Care Med. ;(2)–CrossRef Scholar

  • • Krogulska A, Dynowski J, Jedrzejczyk M, Sardecka I, Malachowska B, Wasowska-Krolikowska K. The impact of food allergens on airway responsiveness in schoolchildren with asthma: A a DBPCFC study. Pediatr Pulmonol.

    ;51(8)– This study shows that food allergens may enhance non-specific bronchial hyperresponsiveness.CrossRef Scholar

  • Ortolani C, Ispano M, Pastorello E, Bigi A, Ansaloni R. The oral allergy syndrome. Ann Allergy. ;61(6 Pt 2)–PubMed Scholar

  • Tuft L, Blumstein G. Studies in food allergy — sensitization to unused fruits: clinical and experimental observations. J Allergy Ther. ;–ef Scholar

  • Webber CM, England RW. Oral allergy syndrome: a clinical, diagnostic, and therapeutic challenge. Ann Allergy Asthma Immunol. ;(2)–8; quiz 9–10, CrossRef Scholar

  • Amlot PL, Kemeny DM, Zachary C, Parkes P, Lessof MH.

    Oral allergy syndrome (OAS): symptoms of IgE-mediated hypersensitivity to foods. Clin Allergy. ;17(1)–CrossRef Scholar

  • van Ree R, Antonicelli L, Akkerdaas JH, Pajno GB, Barberio G, Corbetta L, et al. Asthma after consumption of snails in house-dust-mite-allergic patients: a case of IgE cross-reactivity. Allergy. ;51(6)–CrossRef Scholar

  • Farioli L, Losappio LM, Giuffrida MG, Pravettoni V, Micarelli G, Nichelatti M, et al. Mite-induced asthma and IgE levels to shrimp, mite, tropomyosin, arginine kinase, and Der p 10 are the most risk factors for challenge-provenshrimp allergy. Int Arch Allergy Immunol. ;(3–4)–CrossRef Scholar

  • Roberts G, Golder N, Lack G.

    Bronchial challenges with aerosolized food in asthmatic, food-allergic children. Allergy. ;57(8)–ef Scholar

  • Comstock SS, DeMera R, Vega LC, Boren EJ, Deane S, Haapanen LA, et al. Allergic reactions to peanuts, tree nuts, and seeds aboard commercial airliners. Ann Allergy Asthma Immunol. ;(1)–ef Scholar

  • •• Baur X. A compendium of causative agents of occupational asthma. J Occup Med Toxicol. ;8(1) A comprehensive overview of agents that may induce occupational asthma.CrossRef Scholar

  • Salvatori N, Reccardini F, Convento M, Purinan A, Colle R, De Carli S, et al.

    Asthma induced by inhalation of flour in adults with food allergy to wheat. Clin Exp Allergy. ;38(8)–CrossRef Scholar

  • Campbell CP, Yates DH. Lupin allergy: a hidden killer at home, a menace at work; occupational disease due to lupin allergy. Clin Exp Allergy. ;40(10)–CrossRef Scholar

  • Leser C, Hartmann AL, Praml G, Wuthrich B. The «“egg-egg»” syndrome: occupational respiratory allergy to airborne egg proteins with consecutive ingestive egg allergy in the bakery and confectionery industry. J Investig Allergol Clin Immunol.

    ;11(2)–PubMed

  • Further reading

    1Department of Health, Human Performance and Recreation, Baylor University, Waco, Texas, USA

    *Corresponding Author:Christie Maria Sayes, Environmental Science Department, Baylor University, One Bear Put , Waco, TX ;

    Food allergy, Food sensitivity, Food intolerance, Environment, 10 Essential services

    Discussion

    Individual allergens, their prevalence and diagnoses

    A relatively little quantity of foods are referred to as major food allergens, i.e.

    foods known to elucidate an allergic reaction in humans. These foods include milk, egg, tree nuts, peanuts, seafood, shellfish, soy, and wheat [16]. People can exhibit intolerance to other foods, such as lactose or sulfites; but the adverse reaction to humans after exposure is not described as life threatening.

    Nut allergies (peanut and tree nut) are the leading cause of anaphylaxis, either fatal or nonfatal, in the United States and the United Kingdom [16]. Unlike other food allergens, peanuts are linked to a genetic susceptibility.

    The environmental and physiological precursors to the development of a peanut allergy include early onset of a soy allergy and eczema as an baby, respectfully [17]. In some studies, maternal diet plays a role in the development of a peanut allergy, but other studies own proven this relation untrue [17]. A peanut allergy is unique in that the reaction is chronic and sustained throughout an individual’s life [17].

    According to several studies, the prevalence of food allergies are significantly lower in developing countries than those in developed countries [18].

    However, individuals from developing countries who immigrate to modernized countries lose their protection to certain allergens [18]. The difference between the rates of food allergy onset between developed versus developing countries could be due to factors in the local environmental construct.

    It is hard to pinpoint the rates of allergy prevalence due to the common practice of self- diagnosis, rather than practitioner diagnosis. Allergies can range from a less complicated intolerance or sensitivity to more complicated anaphylaxis. Few studies own been capable to accurately report the prevalence of certain food allergens [19]; and precise diagnosis is directly related to prevalence.

    The most widely accepted method to qualitatively diagnose an allergy is through either a skin test or blood test. Skin allergy testing is a method for medical diagnosis of allergies designed to inflame a controlled irritation response [20]. Blood allergy tests measure the upregulation of immunoglobulin E (IgE, the antibody that triggers food allergy symptoms) to specific foods [21]. In an ideal setting, the test would also include a double-blind, placebo-controlled food challenge (DBPCFC) [22]. More precise prevalence rates for food allergies can be gained with more DBPCFC reported studies.

    Commonality among children

    The onset of food allergies diagnosed among children in the United States own risen 50% since [23].

    Not only own the rates of allergies increased in the past two decades, but the rates of morbidity associated with allergies own risen, as well. Jackson et al. [23] concludes that there is no clear understanding of the reasons for the rising incidence rates; however, the nature of the interaction between genetic and environmental factors requires more research [23].

    Allergy vs. Sensitivity

    Any allergy has the potential to triggers a life threatening immune response. A sensitivity (also referred to as an intolerance) is generally not life threatening, but does result from the inability to metabolize or digest a food completely [22, 25].

    The majority of studies that focus on food allergies tend to avoid the more mild and less complicated food intolerances or sensitivities [26]. There evidence to propose, however, that some food sensitivities can lead to food allergies over time [27] (Figure 2). Most food intolerances and sensitivities are associated with abdominal symptoms such as nausea, bloating, and pain [28]. However, they can also be associated with symptoms such as neurological dysfunction, psychological disturbances, fibromyalgia, and skin rash [29].

    Although there are currently no proven methods to overcome a diagnosed food allergy, there are known ways to overcome a sensitivity related food illness.

    The first step includes completely eliminating the food from the diet, avoidance of the trigger response. The second step includes biochemical restoration. This is the body repairing itself since it is no longer experiencing illness. The third and final step is elimination of bioaccumulated toxicant load. Since the body is no longer experiencing the food item, it is capable to finish rid itself of the toxicants. In some cases, the food at this point can start to be reintroduced to the diet in little amounts.

    The most common food sensitivities include complicated carbohydrates, histamines, and lactase. In carbohydrate intolerance, an essential enzyme is missing from the digestion processes, which causes the incomplete metabolism of fermentable carbohydrates (i.e.

    sugars and starches). In histamine intolerance, foods with large quantity of the chemical histamine (i.e. alcohol, bananas, avocados, or eggplants) cause itchy eyes or tongue, runny nose, or congestion due to a lack of the enzyme diamine oxidase (DAO). In lactose intolerance, the enzyme lactase, responsible for breaking below lactose or milk sugar, is missing and causes diarrhea, nausea, vomiting, abdominal cramps, and bloating [25].

    Known causes and pre-existing health conditions

    There is limited information on the known causes of food allergies. There own been numerous correlations found but only a few studies own proven causation. Asthma and eczema are known pre-existing health conditions that often lead to the development of food allergies [30, 31].

    Generally accepted correlations are listed below:

    Figure 1: The progression of food allergy diagnosis. This figure shows the possible interactions a body can own to an allergen. The three stages are: no sensitivity to the food, food sensitivity, and food allergy.

    Figure 2: Steps to overcome sensitivity related illness.

    Figure 3: (A) Current hypothesized associations between food allergies and external factors and articles associated with them. (B) Greatest number of papers published from search databases used versus the food allergy hypothesis number.

  • 1.

    Lai CK, Beasley R, Crane J, Foliaki S, Shah J, Weiland S, et al.

    Global variation in the prevalence and severity of asthma symptoms: phase three of the International Study of Asthma and Allergies in Childhood (ISAAC). Thorax. ;64(6)–CrossRef Scholar

  • 2.

    Dahlman-Hoglund A, Renstrom A, Larsson PH, Elsayed S, Andersson E. Salmon allergen exposure, occupational asthma, and respiratory symptoms among salmon processing workers. Am J Ind Med. ;55(7)–CrossRef Scholar

  • 3.

    Rona RJ, Keil T, Summers C, Gislason D, Zuidmeer L, Sodergren E, et al. The prevalence of food allergy: a meta-analysis.

    J Allergy Clin Immunol. ;(3)–CrossRef Scholar

  • 4.

    Savage J, Johns CB. Food allergy: epidemiology and natural history. Immunol Allergy Clin N Am. ;35(1)–CrossRef Scholar

  • 5.

    Venter C, Arshad SH. Epidemiology of food allergy. Pediatr Clin N Am. ;58(2)–CrossRef Scholar

  • 6.

    Liu AH, Jaramillo R, Sicherer SH, Wood RA, Bock SA, Burks AW, et al. National prevalence and risk factors for food allergy and relationship to asthma: results from the National Health and Nutrition Examination Survey – J Allergy Clin Immunol.

    ;(4)–CrossRef Scholar

  • 7.

    Arabkhazaeli A, Vijverberg SJ, van Erp FC, Raaijmakers JA, van der Ent CK, van der Maitland Zee AH. Characteristics and severity of asthma in children with and without atopic conditions: a cross-sectional study. BMC Pediatr. ;CrossRef Scholar

  • 8.

    Illi S, von Mutius E, Lau S, Nickel R, Niggemann B, Sommerfeld C, et al. The pattern of atopic sensitization is associated with the development of asthma in childhood. J Allergy Clin Immunol. ;(5)–CrossRef Scholar

  • 9.

    Wang J, Visness CM, Sampson HA. Food allergen sensitization in inner-city children with asthma.

    J Allergy Clin Immunol. ;(5)–CrossRef Scholar

  • Schroeder A, Kumar R, Pongracic JA, Sullivan CL, Caruso DM, Costello J, et al. Food allergy is associated with an increased risk of asthma. Clin Exp Allergy. ;39(2)–CrossRef Scholar

  • Hill DA, Grundmeier RW, Ram G, Spergel JM. The epidemiologic characteristics of healthcare provider-diagnosed eczema, asthma, allergic rhinitis, and food allergy in children: a retrospective cohort study. BMC Pediatr. ;CrossRef Scholar

  • Roberts G, Lack G. Relevance of inhalational exposure to food allergens. Curr Opin Allergy Clin Immunol. ;3(3)–ef Scholar

  • Tariq SM, Matthews SM, Hakim EA, Arshad SH.

    Egg allergy in infancy predicts respiratory allergic disease by 4 years of age. Pediatr Allergy Immunol. ;11(3)–ef Scholar

  • Spergel JM, Paller AS. Atopic dermatitis and the atopic march. J Allergy Clin Immunol. ;(6 Suppl):S–CrossRef Scholar

  • Rhodes HL, Sporik R, Thomas P, Holgate ST, Cogswell JJ. Early life risk factors for adult asthma: a birth cohort study of subjects at risk. J Allergy Clin Immunol. ;(5)–ef Scholar

  • Meyer R, Fleming C, Dominguez-Ortega G, Lindley K, Michaelis L, Thapar N, et al. Manifestations of food protein induced gastrointestinal allergies presenting to a single tertiary paediatric gastroenterology unit.

    World Allergy Organ J. ;6(1)CrossRef Scholar

  • •• Tsakok T, Marrs T, Mohsin M, Baron S, du Toit G, Till S, et al. Does atopic dermatitis cause food allergy? A systematic review. J Allergy Clin Immunol. ;(4)–8. This paper comprises a systematic analysis and review out of 66 research studies. It was concluded that there is a strong association between atopic dermatitis, food sensitization and food allergy.CrossRef Scholar

  • Flohr C, Perkin M, Logan K, Marrs T, Radulovic S, Campbell LE, et al. Atopic dermatitis and disease severity are the main risk factors for food sensitization in exclusively breastfed infants.

    J Invest Dermatol. ;(2)–CrossRef Scholar

  • Guillet G, Guillet MH. Natural history of sensitizations in atopic dermatitis. A 3-year follow-up in children: food allergy and high risk of respiratory symptoms.

    What is the most common food allergy in uk

    Arch Dermatol. ;(2)–CrossRef Scholar

  • Lack G. Epidemiologic risks for food allergy. J Allergy Clin Immunol. ;(6)–ef Scholar

  • Abo-Zaid G, Sharpe RA, Fleming LE, Depledge M, Osborne NJ. Association of baby eczema with childhood and adult asthma: analysis of data from the birth cohort study. Int J Environ Res Public Health. ;15(7).CrossRef Scholar

  • Bergmann RL, Edenharter G, Bergmann KE, Forster J, Bauer CP, Wahn V, et al. Atopic dermatitis in early infancy predicts allergic airway disease at 5 years. Clin Exp Allergy. ;28(8)–CrossRef Scholar

  • Bao Y, Chen Z, Liu E, Xiang L, Zhao D, Hong J.

    Risk factors in preschool children for predicting asthma during the preschool age and the early school age: a systematic review and meta-analysis. Curr Allergy Asthma Rep. ;17(12)CrossRef Scholar

  • Hourihane JO, Dean TP, Warner JO. Peanut allergy in relation to heredity, maternal diet, and other atopic diseases: results of a questionnaire survey, skin prick testing, and food challenges. BMJ. ;()–CrossRef Scholar

  • Sicherer SH, Furlong TJ, Maes HH, Desnick RJ, Sampson HA, Gelb BD.

    Genetics of peanut allergy: a twin study. J Allergy Clin Immunol. ;(1 Pt 1)–ef Scholar

  • Irvine AD, McLean WH, Leung DY. Filaggrin mutations associated with skin and allergic diseases. N Engl J Med. ;(14)–CrossRef Scholar

  • Ziyab AH, Karmaus W, Zhang H, Holloway JW, Steck SE, Ewart S, et al. Allergic sensitization and filaggrin variants predispose to the comorbidity of eczema, asthma, and rhinitis: results from the Isle of Wight birth cohort. Clin Exp Allergy. ;44(9)–ef Scholar

  • Marks GB, Mihrshahi S, Kemp AS, Tovey ER, Webb K, Almqvist C, et al. Prevention of asthma during the first 5 years of life: a randomized controlled trial.

    J Allergy Clin Immunol. ;(1)–CrossRef Scholar

  • Woods RK, Thien F, Raven J, Walters EH, Abramson M. Prevalence of food allergies in young adults and their relationship to asthma, nasal allergies, and eczema. Ann Allergy Asthma Immunol. ;88(2)–ef Scholar

  • Best KP, Sullivan TR, Palmer DJ, Gold M, Martin J, Kennedy D, et al. Prenatal omega-3 LCPUFA and symptoms of allergic disease and sensitization throughout early childhood — a longitudinal analysis of long-term follow-up of a randomized controlled trial.

    World Allergy Organ J. ;11(1)CrossRef Scholar

  • Yepes-Nunez JJ, Brozek JL, Fiocchi A, Pawankar R, Cuello-Garcia C, Zhang Y, et al. Vitamin D supplementation in primary allergy prevention: Systematic systematic review of randomized and non-randomized studies. Allergy. ;73(1)–CrossRef Scholar

  • Kramer MS, Matush L, Vanilovich I, Platt R, Bogdanovich N, Sevkovskaya Z, et al.

    Effect of prolonged and exclusive breast feeding on risk of allergy and asthma: cluster randomised trial. BMJ. ;()CrossRef Scholar

  • Koplin JJ, Osborne NJ, Wake M, Martin PE, Gurrin LC, Robinson MN, et al. Can early introduction of egg prevent egg allergy in infants? A population-based study. J Allergy Clin Immunol. ;(4)–CrossRef Scholar

  • •• Perkin MR, Logan K, Tseng A, Raji B, Ayis S, Peacock J, et al. Randomized trial of introduction of allergenic foods in breast-fed infants. N Engl J Med. ;(18)– This is a RCT in young children in which they show that early introduction of peanut and egg at the age of 3 months results in a reduction of peanut and egg allergy at a later age.CrossRef Scholar

  • Calvani M, Cardinale F, Martelli A, Muraro A, Pucci N, Savino F, et al.

    Risk factors for severe pediatric food anaphylaxis in Italy. Pediatr Allergy Immunol. ;22(8)–ef Scholar

  • Summers CW, Pumphrey RS, Woods CN, McDowell G, Pemberton PW, Arkwright PD. Factors predicting anaphylaxis to peanuts and tree nuts in patients referred to a specialist middle. J Allergy Clin Immunol. ;(3)–ef Scholar

  • Pumphrey RS, Roberts IS. Postmortem findings after fatal anaphylactic reactions. J Clin Pathol. ;53(4)–ef Scholar

  • van Erp FC, Knulst AC, Kentie PA, Pasmans SG, van der Ent CK, Meijer Y. Can we predict severe reactions during peanut challenges in children?

    Pediatr Allergy Immunol. ;24(6)–CrossRef Scholar

  • •• Pettersson ME, Koppelman GH, Flokstra-de Blok BMJ, Kollen BJ, Dubois AEJ. Prediction of the severity of allergic reactions to foods. Allergy. ;73(7)– This study underwrites that the severity of double blind placebo controlled food challenges remains largely unpredictable.CrossRef Scholar

  • Hill DJ, Firer MA, Shelton MJ, Hosking CS. Manifestations of milk allergy in infancy: clinical and immunologic findings. J Pediatr. ;(2)–ef Scholar

  • Bock SA, Munoz-Furlong A, Sampson HA.

    Fatalities due to anaphylactic reactions to foods. J Allergy Clin Immunol. ;(1)–ef Scholar

  • James JM, Eigenmann PA, Eggleston PA, Sampson HA. Airway reactivity changes in asthmatic patients undergoing blinded food challenges. Am J Respir Crit Care Med. ;(2)–CrossRef Scholar

  • • Krogulska A, Dynowski J, Jedrzejczyk M, Sardecka I, Malachowska B, Wasowska-Krolikowska K. The impact of food allergens on airway responsiveness in schoolchildren with asthma: A a DBPCFC study.

    Pediatr Pulmonol. ;51(8)– This study shows that food allergens may enhance non-specific bronchial hyperresponsiveness.CrossRef Scholar

  • Ortolani C, Ispano M, Pastorello E, Bigi A, Ansaloni R. The oral allergy syndrome. Ann Allergy. ;61(6 Pt 2)–PubMed Scholar

  • Tuft L, Blumstein G. Studies in food allergy — sensitization to unused fruits: clinical and experimental observations.

    J Allergy Ther. ;–ef Scholar

  • Webber CM, England RW. Oral allergy syndrome: a clinical, diagnostic, and therapeutic challenge. Ann Allergy Asthma Immunol. ;(2)–8; quiz 9–10, CrossRef Scholar

  • Amlot PL, Kemeny DM, Zachary C, Parkes P, Lessof MH. Oral allergy syndrome (OAS): symptoms of IgE-mediated hypersensitivity to foods. Clin Allergy. ;17(1)–CrossRef Scholar

  • van Ree R, Antonicelli L, Akkerdaas JH, Pajno GB, Barberio G, Corbetta L, et al. Asthma after consumption of snails in house-dust-mite-allergic patients: a case of IgE cross-reactivity.

    Allergy. ;51(6)–CrossRef Scholar

  • Farioli L, Losappio LM, Giuffrida MG, Pravettoni V, Micarelli G, Nichelatti M, et al. Mite-induced asthma and IgE levels to shrimp, mite, tropomyosin, arginine kinase, and Der p 10 are the most risk factors for challenge-provenshrimp allergy. Int Arch Allergy Immunol. ;(3–4)–CrossRef Scholar

  • Roberts G, Golder N, Lack G. Bronchial challenges with aerosolized food in asthmatic, food-allergic children. Allergy. ;57(8)–ef Scholar

  • Comstock SS, DeMera R, Vega LC, Boren EJ, Deane S, Haapanen LA, et al. Allergic reactions to peanuts, tree nuts, and seeds aboard commercial airliners.

    Ann Allergy Asthma Immunol. ;(1)–ef Scholar

  • •• Baur X. A compendium of causative agents of occupational asthma. J Occup Med Toxicol. ;8(1) A comprehensive overview of agents that may induce occupational asthma.CrossRef Scholar

  • Salvatori N, Reccardini F, Convento M, Purinan A, Colle R, De Carli S, et al. Asthma induced by inhalation of flour in adults with food allergy to wheat. Clin Exp Allergy. ;38(8)–CrossRef Scholar

  • Campbell CP, Yates DH. Lupin allergy: a hidden killer at home, a menace at work; occupational disease due to lupin allergy.

    Clin Exp Allergy. ;40(10)–CrossRef Scholar

  • Leser C, Hartmann AL, Praml G, Wuthrich B. The «“egg-egg»” syndrome: occupational respiratory allergy to airborne egg proteins with consecutive ingestive egg allergy in the bakery and confectionery industry. J Investig Allergol Clin Immunol. ;11(2)–PubMed

  • Further reading

    1Department of Health, Human Performance and Recreation, Baylor University, Waco, Texas, USA

    *Corresponding Author:Christie Maria Sayes, Environmental Science Department, Baylor University, One Bear Put , Waco, TX ;

    Food allergy, Food sensitivity, Food intolerance, Environment, 10 Essential services

    Discussion

    Individual allergens, their prevalence and diagnoses

    A relatively little quantity of foods are referred to as major food allergens, i.e.

    foods known to elucidate an allergic reaction in humans. These foods include milk, egg, tree nuts, peanuts, seafood, shellfish, soy, and wheat [16]. People can exhibit intolerance to other foods, such as lactose or sulfites; but the adverse reaction to humans after exposure is not described as life threatening.

    Nut allergies (peanut and tree nut) are the leading cause of anaphylaxis, either fatal or nonfatal, in the United States and the United Kingdom [16]. Unlike other food allergens, peanuts are linked to a genetic susceptibility.

    The environmental and physiological precursors to the development of a peanut allergy include early onset of a soy allergy and eczema as an baby, respectfully [17]. In some studies, maternal diet plays a role in the development of a peanut allergy, but other studies own proven this relation untrue [17]. A peanut allergy is unique in that the reaction is chronic and sustained throughout an individual’s life [17].

    According to several studies, the prevalence of food allergies are significantly lower in developing countries than those in developed countries [18].

    However, individuals from developing countries who immigrate to modernized countries lose their protection to certain allergens [18]. The difference between the rates of food allergy onset between developed versus developing countries could be due to factors in the local environmental construct.

    It is hard to pinpoint the rates of allergy prevalence due to the common practice of self- diagnosis, rather than practitioner diagnosis. Allergies can range from a less complicated intolerance or sensitivity to more complicated anaphylaxis. Few studies own been capable to accurately report the prevalence of certain food allergens [19]; and precise diagnosis is directly related to prevalence.

    The most widely accepted method to qualitatively diagnose an allergy is through either a skin test or blood test. Skin allergy testing is a method for medical diagnosis of allergies designed to inflame a controlled irritation response [20]. Blood allergy tests measure the upregulation of immunoglobulin E (IgE, the antibody that triggers food allergy symptoms) to specific foods [21]. In an ideal setting, the test would also include a double-blind, placebo-controlled food challenge (DBPCFC) [22]. More precise prevalence rates for food allergies can be gained with more DBPCFC reported studies.

    Commonality among children

    The onset of food allergies diagnosed among children in the United States own risen 50% since [23].

    Not only own the rates of allergies increased in the past two decades, but the rates of morbidity associated with allergies own risen, as well. Jackson et al. [23] concludes that there is no clear understanding of the reasons for the rising incidence rates; however, the nature of the interaction between genetic and environmental factors requires more research [23].

    Allergy vs. Sensitivity

    Any allergy has the potential to triggers a life threatening immune response. A sensitivity (also referred to as an intolerance) is generally not life threatening, but does result from the inability to metabolize or digest a food completely [22, 25]. The majority of studies that focus on food allergies tend to avoid the more mild and less complicated food intolerances or sensitivities [26].

    There evidence to propose, however, that some food sensitivities can lead to food allergies over time [27] (Figure 2). Most food intolerances and sensitivities are associated with abdominal symptoms such as nausea, bloating, and pain [28]. However, they can also be associated with symptoms such as neurological dysfunction, psychological disturbances, fibromyalgia, and skin rash [29].

    Although there are currently no proven methods to overcome a diagnosed food allergy, there are known ways to overcome a sensitivity related food illness.

    The first step includes completely eliminating the food from the diet, avoidance of the trigger response. The second step includes biochemical restoration. This is the body repairing itself since it is no longer experiencing illness. The third and final step is elimination of bioaccumulated toxicant load. Since the body is no longer experiencing the food item, it is capable to finish rid itself of the toxicants. In some cases, the food at this point can start to be reintroduced to the diet in little amounts.

    The most common food sensitivities include complicated carbohydrates, histamines, and lactase.

    In carbohydrate intolerance, an essential enzyme is missing from the digestion processes, which causes the incomplete metabolism of fermentable carbohydrates (i.e. sugars and starches). In histamine intolerance, foods with large quantity of the chemical histamine (i.e. alcohol, bananas, avocados, or eggplants) cause itchy eyes or tongue, runny nose, or congestion due to a lack of the enzyme diamine oxidase (DAO). In lactose intolerance, the enzyme lactase, responsible for breaking below lactose or milk sugar, is missing and causes diarrhea, nausea, vomiting, abdominal cramps, and bloating [25].

    Known causes and pre-existing health conditions

    There is limited information on the known causes of food allergies.

    There own been numerous correlations found but only a few studies own proven causation. Asthma and eczema are known pre-existing health conditions that often lead to the development of food allergies [30, 31]. Generally accepted correlations are listed below:

    • Eczema in infants is an early indicator to the presence of a food allergy [32].
    • Individuals with asthma tend to own a food allergy [16].
    • Children tend to own more than one food allergy present at a time [17].
    • Genetic history of food allergies can increase the risk for developing a food allergy tenfold [16, 21].

    A few relationships between environmental factors and food allergies that own been studied but are inconclusive and often debated:

    A few relationships between environmental factors and food allergies that own been studied but are inconclusive and often debated:

    • A higher body mass index (BMI) is associated with an increased risk of allergies in children; however, the association varies depending on gender, age, and type of allergen [33].
    • Some foods prepared and eaten raw (uncooked) induce adverse allergic reactions; however, some of the same foods prepared and eaten cooked also induce the same reaction [34].
    • Antibiotic use in children, as well as lack of healthy commensal bacteria has shown to be a risk factor for developing food allergies; but, the trends in observed data are not general [35].

    Results

    Using this search strategy, we identified a entire of unique articles in English, while carefully eliminating any frequencies in search results among and between the search engines employed.

    After other exclusion criteria were accounted for, 11 articles remained for review. The bibliographies of these 11 papers were also examined for additional relevant articles, but relevant cited articles were already captured in the initial analyses. These articles are limited to research studies with experimental designs and are summarized in Table 2. Our analysis is outlined as follows: first, brief overviews of Individual allergens, their prevalence and diagnoses; historical perspectives (Current era vs.

    past eras), discussion of Allergy vs. intolerance/sensitivity, and Known causes and pre-existing health conditions are discussed. Second, the five working hypotheses in this field of study are explained. Third, the environmental factors contributing to the onset of food allergies are proposed.

    Paper Reference

    Brief Study Design

    Environmental Factor
    Measure

    Human Health
    Measure

    Result

    Gern et al.

    [5]

    Pet exposure in the home
    compared against
    cytokine secretion in infants

    Dogs

    Indicators of atopy

    Having a dog in infancy is
    associated with higher
    cytokine secretion
    profiles and reduced allergic
    sensitization

    Kilpelainen et al. [7]

    Self-reported wheezing from
    Finnish students
    ( yr.) collected via
    questionnaire

    Childhood farm
    environment

    Food allergy,
    allergic
    rhinitis and/or
    allergic
    conjunctivitis

    The childhood farm
    environment independently
    reduced the risk for physician-
    diagnosed allergies

    Liu et al.

    [8]

    Sensitization measured by
    skin prick on Chinese
    twin pairs ( yr.)

    Living conditions,
    environment,

    and genetics

    Peanut and
    shellfish food
    sensitization

    Sensitivity to common food
    allergens is influenced
    by genetic and
    environmental f actors

    Leynaert et al. [6]

    Questionnaire on farm
    exposure in childhood in
    2 French centers

    Childhood farm
    environment &
    D14 CT
    polymorphism

    Atopic
    sensitization

    CD14 CT and farm
    childhood environment
    exposure may
    modify the development
    of atopy

    Simpson et al.

    [9]

    Population-based birth
    cohort study

    Endotoxin in
    home dust

    Allergic
    sensitization
    and eczema

    Increasing endotoxin exposure
    is associated
    with reduced risk of
    allergic sensitization

    Melén et al. [3]

    Birth cohort study

    Air pollution from
    local traffic

    Allergic
    disease and
    inflammatory
    response

    Long term exposure to
    traffic pollutions
    can increase allergy
    sensitization

    Lawlis et al. [10]

    Online survey of principals
    on school allergy awareness

    School environment

    Food-induced
    allergic
    reactions
    (i.e.

    anaphylaxis)
    from milk, eggs,
    peanuts,& seafood

    Detailed awareness and
    management
    guidelines are integral for
    schools to adequately
    manage foodinduced allergic
    reactions, in the
    school environment

    Makhija
    et al. [11]

    Questionnaires on home
    demographics of mothers
    and fathers of food allergic
    children

    Home environment
    and
    demographic
    characteristics

    Eczema, atopic
    diseases, & food
    allergies

    Parents of food allergic
    children found
    higher rates of sensitization to
    foods and aeroallergens
    compared with the
    general population

    Majowicz
    et al.

    [12]

    Conceptual model

    Built and natural
    environment

    Foodborne illness,
    food insecurity,
    obesity, & food
    allergy

    Health practitioners should
    consider how targeted
    public health actions produce
    positive or negative population
    health impacts

    Ben- Shoshan
    et al. [13]

    Telephone survey of individuals
    with probable self
    reported food allergies

    Personal/family
    history of atopy,
    sociodemographi cs,
    & lifestyle habits

    Food allergy (i.e.
    milk, egg,
    peanut, tree nut,
    shellfish, fish,
    wheat, soy,
    or sesame)

    Development of eczema in
    the first 2 years of
    life is consistently
    associated with food allergies

    Bedolla- Barajas
    et al.

    [14]

    Questionnaire to parents of
    children ( yr.)
    needing allergy treatment

    Demographic and
    clinical
    data history

    Oral allergy
    syndrome
    (OAS)

    OAS is not uncommon
    in our
    environment; pineapple was the
    main food related .
    Quercus sp. was the pollen
    associated

    Xu et al. [15]

    Questionnaire to parents
    of Chinese
    children ( yr.)
    with atopic dermatitis

    Home environment

    Atopic
    dermatitis

    Home renovation/ redecoration,
    new furniture, indoor mold,
    urban residency, heredity
    disposition and
    food allergy can be risk factors for
    childhood allergy development

    Table 2: Summary of the research articles from the peer-reviewed literature that relates an environmental factor to the onset of an allergic reaction, sensitization, or disease.

    Introduction

    Approximately 50 million Americans experience a food allergy.

    Food allergies affect up to six percent (6%) of children and four percent (4%) of adults (ACAAI ). Food allergies can develop at any age, but typically appear first during infancy or childhood (ACAAI ). However, in some occasions, an individual can develop an allergy, and subsequent adverse effect, to a food they own previously eaten with no negative symptoms (ACAAI ). In a
    recent study released by the Middle for Disease Control (), it was reported that between the years of and , food allergies among children increased 50% (CDC ). The number of food allergies is increasing, but the cause is unknown. The rate of anaphylaxis reactions after exposure to food is increasing, as well [1].

    Anaphylactic reactions can be deadly if not immediately treated; key signs are facial swelling and difficulty breathing cause is unknown [1].

    Little data is available that postulates the causes of food allergies. However, some hypotheses own emerged over the past 10 years. For instance, factors such as race, ethnicity, and genetics contribute to allergy development (ACAAI ). More recently, research efforts own shifted from genetic-centric to synergistic reasoning incorporating environmental factors. Another striking statistic emerging in the literature over the past 5 years is the overwhelmingly high rates of food allergy development among individuals residing in first world countries, as compared to individuals who live in third world countries [2].

    It has been postulated that the highly variable environmental factors in an industrialized nation contributes to the increase in the onset of food allergy [3].

    Food allergy conditions are a complicated diagnosis; each individual is affected differently. It is also a hard area of epidemiological, toxicological, or medicinal research because numerous food allergies are self-reported without qualifying or quantifying metrics (such as pathology, symptom, or biomarker identification).

    To complicate the subject further, a food allergy can exist along a continuum (or spectrum). Figure 1 describes the spectrum of food disorder; an Individual can own ‘no sensitivity’, food ‘sensitivity’, and/or a food ‘allergy’ to a food product. A food allergy is generally regarded as the more severe diseased state and induces an exaggerated immune response. Lastly, the allergic reaction to a food can vary among inflicted individuals. Example conditions arising from a food allergy could range from itching skin to urticarial outbreak to gastrointestinal dysfunction to anaphylaxis (CDC ).

    Literature presents the possible correlation between the environment and an increase in allergies.

    While no literature has yet to prove causation, a few articles own proposed possible correlations. Within the environmental construct of food and food delivery, the individual’s culture often promotes specific allergic reactions; if a food is not eaten in the population, then tolerance to the food is never developed, thus can result in a food allergy. A few significant research studies published in the literature own postulated that environmental factors influence the onset of food allergies, but extremely few own collected empirical data suggesting causation. Without causations and known ways to prevent food allergies, the epidemic will continue to grow and continue to adversely affect millions of people.

    A country’s food system can present itself as a cause to an allergen being present in the country or not. The dual-allergen-exposure hypothesis hypothesizes that in countries where a food is not consumed, there is no environmental exposure, an allergy to that food will not happen [4]. An example of this occurred in the United Kingdom. Prior to , kiwis had never been present or eaten in the UK. Since the ’s when the kiwi was introduced to the UK, the rate of kiwi allergies has grown significantly [4].

    Another possible hypothesis could be in countries where they avoid a certain food i.e. peanuts, the rates of peanut allergies tend to be higher.

    There’s a misunderstanding that by completely avoiding and not introducing an infant/child to the item, they won’t develop an allergy. However, we’ve seen in America that this proves the opposite. Consequently, countries such as in Africa and some Asian countries where peanuts are widely eaten and avoided, there are extremely low rates of peanut allergies [4]. Researchers know that the environment plays a role in the development of food allergies, but few own studies own found concrete evidence to support the role that the environment plays.

    Some possible roles the environment contributes to food allergies include: traffic pollution, animal exposure, farm environment, smoking, and air pollution. One study reviewed found that long-term exposure to traffic pollutions can increase allergy sensitization [3]. The study looked at children. One possibility of this correlation could be the knowledge that exposure to traffic and air pollution can increase rates of asthma which therefore can increase the rates of food allergies.

    Another study looked at the effects of dog ownership on the development of atopy among infants. It found that households that had a dog, the infants residing in these houses, were less likely to develop atopic dermatitis. This could appear in the form of eczema. It found that these results only proved true with dogs though, cats were evaluated as well but found to own no effect on the development of atopy [5].

    Two studies indicated evidence that early exposure to a farm environment could lower the risk of a kid developing atopy in the future.

    One study found that living on a farm in the early years helped to lift rates of genotype CD Low CD14 levels are associated with an increased risk of developing atopic sensitization. This study showed that the farm environment contributed to higher rates of CD14 among infants therefore, the infants had a lower risk of developing atopy [6]. Another study on farm environment found that a farm environment was successful in preventing allergic rhinitis (hay fever) and allergic conjunctivitis (itching eyes), but not allergic dermatitis (eczema) [7].

    Allergic rhinitis and allergic conjunctivitis do not lead to the development of food allergies. More research needs to be done on the protective factors of a farm environment and the development of food allergies.

    Air pollution can be another cause of developing food allergies. A study found that passive or athletic smoking could frolic a role in the sensitization to food allergens. Passive smoking is inhalation of second-hand smoke and athletic smoking is a person who smokes.

    The same study found that exposure to aeroallergens or air pollutants can cause higher rates of respiratory infections which in turn might frolic an significant role in the sensitization to food allergens as well [8].

    The purpose of this review is to examine environmental factors as a cause of food allergies. First, we attempted to identify environmental factors that contribute to the increasing prevalence of food allergies in the past two decades. Second, we summarized the role that physiological factors (such as genetics, gender, and age) own played in the development of food allergies. Third, we evaluated the importance of the 10 Essential Services of Public Health in food allergy causation.

    The objective of this paper is to define the role of the environment as it relates to food allergies. If environmental factors contribute to the onset of food allergies, then this epidemic could be labeled as an emerging public health issue.

    Methods

    We performed a structured literature search focused on identifying every relevant human studies related to environmental factors and food allergies. Multiple databases were queried between November and May PubMed, Scopus, and Web of Science search engines were utilized with keyword searches. Papers were included if they were tagged with at least one search term from Group A and the term “environment*” from Group term B (Table 1).

    Further literature research narrowed the field to pediatric relevance. The most common themes identified from the original Group B term included: environmental factors, farm environment, smoking, and air pollution. Resultant papers written in English, found in the keyword search, and peer-reviewed were included in the analysis. Searches included both research and review articles on humans, but excluded articles using animal or cell-based models. Other inclusion criteria include specific environmental factors noted in abstract and cohorts of children or young adults.

    Databases

    Group A terms

    Group B terms

    Number of papers returned

    PubMed

    food allergy

    environment*

    food sensitivity

    1

    food intolerance

    9

    Scopus

    food allergy

    environment*

    food sensitivity

    4

    food intolerance

    23

    Web of Science

    food allergy

    environment*

    food sensitivity

    1

    food intolerance

    10

    Table 1: Search terms for literature review.

    *indicates end-truncated search term. Terms entered into database with quotation marks returned results with exact matches. Data includes both research and review articles.

    References

    Results

    Using this search strategy, we identified a entire of unique articles in English, while carefully eliminating any frequencies in search results among and between the search engines employed. After other exclusion criteria were accounted for, 11 articles remained for review.

    The bibliographies of these 11 papers were also examined for additional relevant articles, but relevant cited articles were already captured in the initial analyses. These articles are limited to research studies with experimental designs and are summarized in Table 2. Our analysis is outlined as follows: first, brief overviews of Individual allergens, their prevalence and diagnoses; historical perspectives (Current era vs. past eras), discussion of Allergy vs. intolerance/sensitivity, and Known causes and pre-existing health conditions are discussed.

    Second, the five working hypotheses in this field of study are explained. Third, the environmental factors contributing to the onset of food allergies are proposed.

    Paper Reference

    Brief Study Design

    Environmental Factor
    Measure

    Human Health
    Measure

    Result

    Gern et al. [5]

    Pet exposure in the home
    compared against
    cytokine secretion in infants

    Dogs

    Indicators of atopy

    Having a dog in infancy is
    associated with higher
    cytokine secretion
    profiles and reduced allergic
    sensitization

    Kilpelainen et al.

    [7]

    Self-reported wheezing from
    Finnish students
    ( yr.) collected via
    questionnaire

    Childhood farm
    environment

    Food allergy,
    allergic
    rhinitis and/or
    allergic
    conjunctivitis

    The childhood farm
    environment independently
    reduced the risk for physician-
    diagnosed allergies

    Liu et al.

    [8]

    Sensitization measured by
    skin prick on Chinese
    twin pairs ( yr.)

    Living conditions,
    environment,

    and genetics

    Peanut and
    shellfish food
    sensitization

    Sensitivity to common food
    allergens is influenced
    by genetic and
    environmental f actors

    Leynaert et al. [6]

    Questionnaire on farm
    exposure in childhood in
    2 French centers

    Childhood farm
    environment &
    D14 CT
    polymorphism

    Atopic
    sensitization

    CD14 CT and farm
    childhood environment
    exposure may
    modify the development
    of atopy

    Simpson et al.

    [9]

    Population-based birth
    cohort study

    Endotoxin in
    home dust

    Allergic
    sensitization
    and eczema

    Increasing endotoxin exposure
    is associated
    with reduced risk of
    allergic sensitization

    Melén et al. [3]

    Birth cohort study

    Air pollution from
    local traffic

    Allergic
    disease and
    inflammatory
    response

    Long term exposure to
    traffic pollutions
    can increase allergy
    sensitization

    Lawlis et al.

    [10]

    Online survey of principals
    on school allergy awareness

    School environment

    Food-induced
    allergic
    reactions
    (i.e. anaphylaxis)
    from milk, eggs,
    peanuts,& seafood

    Detailed awareness and
    management
    guidelines are integral for
    schools to adequately
    manage foodinduced allergic
    reactions, in the
    school environment

    Makhija
    et al. [11]

    Questionnaires on home
    demographics of mothers
    and fathers of food allergic
    children

    Home environment
    and
    demographic
    characteristics

    Eczema, atopic
    diseases, & food
    allergies

    Parents of food allergic
    children found
    higher rates of sensitization to
    foods and aeroallergens
    compared with the
    general population

    Majowicz
    et al.

    [12]

    Conceptual model

    Built and natural
    environment

    Foodborne illness,
    food insecurity,
    obesity, & food
    allergy

    Health practitioners should
    consider how targeted
    public health actions produce
    positive or negative population
    health impacts

    Ben- Shoshan
    et al. [13]

    Telephone survey of individuals
    with probable self
    reported food allergies

    Personal/family
    history of atopy,
    sociodemographi cs,
    & lifestyle habits

    Food allergy (i.e.
    milk, egg,
    peanut, tree nut,
    shellfish, fish,
    wheat, soy,
    or sesame)

    Development of eczema in
    the first 2 years of
    life is consistently
    associated with food allergies

    Bedolla- Barajas
    et al.

    [14]

    Questionnaire to parents of
    children ( yr.)
    needing allergy treatment

    Demographic and
    clinical
    data history

    Oral allergy
    syndrome
    (OAS)

    OAS is not uncommon
    in our
    environment; pineapple was the
    main food related .

    What is the most common food allergy in uk

    Quercus sp. was the pollen
    associated

    Xu et al. [15]

    Questionnaire to parents
    of Chinese
    children ( yr.)
    with atopic dermatitis

    Home environment

    Atopic
    dermatitis

    Home renovation/ redecoration,
    new furniture, indoor mold,
    urban residency, heredity
    disposition and
    food allergy can be risk factors for
    childhood allergy development

    Table 2: Summary of the research articles from the peer-reviewed literature that relates an environmental factor to the onset of an allergic reaction, sensitization, or disease.

    Introduction

    Approximately 50 million Americans experience a food allergy.

    Food allergies affect up to six percent (6%) of children and four percent (4%) of adults (ACAAI ). Food allergies can develop at any age, but typically appear first during infancy or childhood (ACAAI ). However, in some occasions, an individual can develop an allergy, and subsequent adverse effect, to a food they own previously eaten with no negative symptoms (ACAAI ). In a
    recent study released by the Middle for Disease Control (), it was reported that between the years of and , food allergies among children increased 50% (CDC ).

    The number of food allergies is increasing, but the cause is unknown. The rate of anaphylaxis reactions after exposure to food is increasing, as well [1]. Anaphylactic reactions can be deadly if not immediately treated; key signs are facial swelling and difficulty breathing cause is unknown [1].

    Little data is available that postulates the causes of food allergies. However, some hypotheses own emerged over the past 10 years. For instance, factors such as race, ethnicity, and genetics contribute to allergy development (ACAAI ).

    More recently, research efforts own shifted from genetic-centric to synergistic reasoning incorporating environmental factors. Another striking statistic emerging in the literature over the past 5 years is the overwhelmingly high rates of food allergy development among individuals residing in first world countries, as compared to individuals who live in third world countries [2]. It has been postulated that the highly variable environmental factors in an industrialized nation contributes to the increase in the onset of food allergy [3].

    Food allergy conditions are a complicated diagnosis; each individual is affected differently.

    It is also a hard area of epidemiological, toxicological, or medicinal research because numerous food allergies are self-reported without qualifying or quantifying metrics (such as pathology, symptom, or biomarker identification). To complicate the subject further, a food allergy can exist along a continuum (or spectrum). Figure 1 describes the spectrum of food disorder; an Individual can own ‘no sensitivity’, food ‘sensitivity’, and/or a food ‘allergy’ to a food product.

    A food allergy is generally regarded as the more severe diseased state and induces an exaggerated immune response. Lastly, the allergic reaction to a food can vary among inflicted individuals. Example conditions arising from a food allergy could range from itching skin to urticarial outbreak to gastrointestinal dysfunction to anaphylaxis (CDC ).

    Literature presents the possible correlation between the environment and an increase in allergies. While no literature has yet to prove causation, a few articles own proposed possible correlations.

    Within the environmental construct of food and food delivery, the individual’s culture often promotes specific allergic reactions; if a food is not eaten in the population, then tolerance to the food is never developed, thus can result in a food allergy. A few significant research studies published in the literature own postulated that environmental factors influence the onset of food allergies, but extremely few own collected empirical data suggesting causation. Without causations and known ways to prevent food allergies, the epidemic will continue to grow and continue to adversely affect millions of people.

    A country’s food system can present itself as a cause to an allergen being present in the country or not. The dual-allergen-exposure hypothesis hypothesizes that in countries where a food is not consumed, there is no environmental exposure, an allergy to that food will not happen [4]. An example of this occurred in the United Kingdom. Prior to , kiwis had never been present or eaten in the UK. Since the ’s when the kiwi was introduced to the UK, the rate of kiwi allergies has grown significantly [4].

    Another possible hypothesis could be in countries where they avoid a certain food i.e. peanuts, the rates of peanut allergies tend to be higher.

    There’s a misunderstanding that by completely avoiding and not introducing an infant/child to the item, they won’t develop an allergy. However, we’ve seen in America that this proves the opposite. Consequently, countries such as in Africa and some Asian countries where peanuts are widely eaten and avoided, there are extremely low rates of peanut allergies [4]. Researchers know that the environment plays a role in the development of food allergies, but few own studies own found concrete evidence to support the role that the environment plays. Some possible roles the environment contributes to food allergies include: traffic pollution, animal exposure, farm environment, smoking, and air pollution.

    One study reviewed found that long-term exposure to traffic pollutions can increase allergy sensitization [3]. The study looked at children. One possibility of this correlation could be the knowledge that exposure to traffic and air pollution can increase rates of asthma which therefore can increase the rates of food allergies. Another study looked at the effects of dog ownership on the development of atopy among infants. It found that households that had a dog, the infants residing in these houses, were less likely to develop atopic dermatitis.

    This could appear in the form of eczema. It found that these results only proved true with dogs though, cats were evaluated as well but found to own no effect on the development of atopy [5].

    Two studies indicated evidence that early exposure to a farm environment could lower the risk of a kid developing atopy in the future. One study found that living on a farm in the early years helped to lift rates of genotype CD Low CD14 levels are associated with an increased risk of developing atopic sensitization. This study showed that the farm environment contributed to higher rates of CD14 among infants therefore, the infants had a lower risk of developing atopy [6].

    Another study on farm environment found that a farm environment was successful in preventing allergic rhinitis (hay fever) and allergic conjunctivitis (itching eyes), but not allergic dermatitis (eczema) [7]. Allergic rhinitis and allergic conjunctivitis do not lead to the development of food allergies. More research needs to be done on the protective factors of a farm environment and the development of food allergies.

    Air pollution can be another cause of developing food allergies. A study found that passive or athletic smoking could frolic a role in the sensitization to food allergens. Passive smoking is inhalation of second-hand smoke and athletic smoking is a person who smokes.

    The same study found that exposure to aeroallergens or air pollutants can cause higher rates of respiratory infections which in turn might frolic an significant role in the sensitization to food allergens as well [8].

    The purpose of this review is to examine environmental factors as a cause of food allergies. First, we attempted to identify environmental factors that contribute to the increasing prevalence of food allergies in the past two decades. Second, we summarized the role that physiological factors (such as genetics, gender, and age) own played in the development of food allergies.

    Third, we evaluated the importance of the 10 Essential Services of Public Health in food allergy causation. The objective of this paper is to define the role of the environment as it relates to food allergies. If environmental factors contribute to the onset of food allergies, then this epidemic could be labeled as an emerging public health issue.

    Methods

    We performed a structured literature search focused on identifying every relevant human studies related to environmental factors and food allergies.

    Multiple databases were queried between November and May PubMed, Scopus, and Web of Science search engines were utilized with keyword searches. Papers were included if they were tagged with at least one search term from Group A and the term “environment*” from Group term B (Table 1). Further literature research narrowed the field to pediatric relevance. The most common themes identified from the original Group B term included: environmental factors, farm environment, smoking, and air pollution. Resultant papers written in English, found in the keyword search, and peer-reviewed were included in the analysis.

    Searches included both research and review articles on humans, but excluded articles using animal or cell-based models. Other inclusion criteria include specific environmental factors noted in abstract and cohorts of children or young adults.

    Databases

    Group A terms

    Group B terms

    Number of papers returned

    PubMed

    food allergy

    environment*

    food sensitivity

    1

    food intolerance

    9

    Scopus

    food allergy

    environment*

    food sensitivity

    4

    food intolerance

    23

    Web of Science

    food allergy

    environment*

    food sensitivity

    1

    food intolerance

    10

    Table 1: Search terms for literature review.

    *indicates end-truncated search term. Terms entered into database with quotation marks returned results with exact matches. Data includes both research and review articles.

    References

    • Milner JD, Stein DM, McCarter R, et al. Early baby multivitamin supplementation is associated with increased risk for food allergy and asthma. Pediatrics ():
    • Camargo CA, Clark S, Kaplan MS, et al. Regional differences in epipen prescriptions in the United States: The potential role of vitamin d. Journal of Allergy and Clinical Immunology ():
    • Bock SA, Munoz-Furlong A, Sampson HA.

      Fatalities due to anaphylactic reactions to foods. J Allergy Clin Immunol. ;(1)–ef Scholar

    • Ben-Shoshan M, Soller L, Harrington DW, et al. Eczema in early childhood, sociodemographic factors and lifestyle habits are associated with food allergy: A nested case-control study. International Archives of Allergy and Immunology ():
    • Tuft L, Blumstein G. Studies in food allergy — sensitization to unused fruits: clinical and experimental observations. J Allergy Ther. ;–ef Scholar

    • Ortolani C, Ispano M, Pastorello E, Bigi A, Ansaloni R.

      The oral allergy syndrome. Ann Allergy. ;61(6 Pt 2)–PubMed Scholar

    • •• Tsakok T, Marrs T, Mohsin M, Baron S, du Toit G, Till S, et al. Does atopic dermatitis cause food allergy? A systematic review. J Allergy Clin Immunol. ;(4)–8. This paper comprises a systematic analysis and review out of 66 research studies. It was concluded that there is a strong association between atopic dermatitis, food sensitization and food allergy.CrossRef Scholar

    • Koplin JJ, Osborne NJ, Wake M, Martin PE, Gurrin LC, Robinson MN, et al. Can early introduction of egg prevent egg allergy in infants? A population-based study. J Allergy Clin Immunol.

      ;(4)–CrossRef Scholar

    • Schroeder A, Kumar R, Pongracic JA, Sullivan CL, Caruso DM, Costello J, et al. Food allergy is associated with an increased risk of asthma. Clin Exp Allergy. ;39(2)–CrossRef Scholar

    • Calvani M, Cardinale F, Martelli A, Muraro A, Pucci N, Savino F, et al. Risk factors for severe pediatric food anaphylaxis in Italy. Pediatr Allergy Immunol. ;22(8)–ef Scholar

    • Aziz I, Hadjivassiliou M, Sanders DS. The spectrum of noncoeliac gluten sensitivity. Nature Reviews Gastroenterology & Hepatology 12 ():
    • van Erp FC, Knulst AC, Kentie PA, Pasmans SG, van der Ent CK, Meijer Y.

      Can we predict severe reactions during peanut challenges in children? Pediatr Allergy Immunol. ;24(6)–CrossRef Scholar

    • Gern JE, Reardon CL, Hoffjan S, et al. Effects of dog ownership and genotype on immune development and atopy in infancy. Journal of Allergy and Clinical Immunology ():
    • von Mutius E. The environmental predictors of allergic disease. Journal of Allergy and Clinical Immunology ():
    • Lack G. Epidemiologic risks for food allergy. J Allergy Clin Immunol. ;(6)–ef Scholar

    • Misselwitz B, Pohl D, Frühauf H, et al. Lactose malabsorption and intolerance: Pathogenesis, diagnosis and treatment. United European Gastroenterology Journal 1 ():
    • Abo-Zaid G, Sharpe RA, Fleming LE, Depledge M, Osborne NJ.

      Association of baby eczema with childhood and adult asthma: analysis of data from the birth cohort study. Int J Environ Res Public Health. ;15(7).CrossRef Scholar

    • Marklund B, Ahlstedt S, Nordström G. Health-related quality of life among adolescents with allergy-like conditions?with emphasis on food hypersensitivity. Health and Quality of Life Outcomes 2 ():
    • Lawlis T, Bakonyi S, Williams LT. Food allergy in schools: The importance of government involvement.

      Nutrition and Dietetics ().

    • Sicherer SH, Muñoz-Furlong A, Godbold JH, et al. Us prevalence of self-reported peanut, tree nut, and sesame allergy: year follow-up. Journal of Allergy and Clinical Immunology ():
    • Sampson HA. Update on food allergy. Journal of Allergy and Clinical Immunology ():
    • •• Baur X. A compendium of causative agents of occupational asthma. J Occup Med Toxicol. ;8(1) A comprehensive overview of agents that may induce occupational asthma.CrossRef Scholar

    • Sicherer SH, Sampson HA. Food allergy. Journal of Allergy and Clinical Immunology (): SS
    • Hill DA, Grundmeier RW, Ram G, Spergel JM.

      The epidemiologic characteristics of healthcare provider-diagnosed eczema, asthma, allergic rhinitis, and food allergy in children: a retrospective cohort study. BMC Pediatr. ;CrossRef Scholar

    • Gupta RS, Springston EE, Warrier MR, et al. The prevalence, severity, and distribution of childhood food allergy in the United States. Pediatrics:peds ():
    • Kim JS, Sinacore JM, Pongracic JA. Parental use of epipen for children with food allergies. Journal of Allergy and Clinical Immunology ():
    • Sporik R, Hill DJ, Hosking CS.

      Specificity of allergen skin testing in predicting positive open food challenges to milk, egg and peanut in children. Clinical & Experimental Allergy 30 ():

    • Rona RJ, Keil T, Summers C, et al. The prevalence of food allergy: A meta-analysis. Journal of Allergy and Clinical Immunology ():
    • Lack G. Epidemiologic risks for food allergy. Journal of Allergy and Clinical Immunology ():
    • • Krogulska A, Dynowski J, Jedrzejczyk M, Sardecka I, Malachowska B, Wasowska-Krolikowska K. The impact of food allergens on airway responsiveness in schoolchildren with asthma: A a DBPCFC study.

      Pediatr Pulmonol. ;51(8)– This study shows that food allergens may enhance non-specific bronchial hyperresponsiveness.CrossRef Scholar

    • Bock SA, Muñoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. Journal of Allergy and Clinical Immunology ():
    • Leynaert B, Guilloud-Bataille M, Soussan D, et al. Association between farm exposure and atopy, according to the cd14 ct polymorphism.

      Journal of Allergy and Clinical Immunology ():

    • Weiss C, Muñoz-Furlong A, Furlong TJ, et al. Impact of food allergies on school nursing practice. The Journal of School Nursing 20 ():
    • Primeau MN, Kagan R, Joseph L, et al. The psychological burden of peanut allergy as perceived by adults with peanut allergy and the parents of peanut- allergic children. Clinical and Experimental Allergy 30 ():
    • Summers CW, Pumphrey RS, Woods CN, McDowell G, Pemberton PW, Arkwright PD.

      Factors predicting anaphylaxis to peanuts and tree nuts in patients referred to a specialist middle. J Allergy Clin Immunol. ;(3)–ef Scholar

    • 5.

      Venter C, Arshad SH. Epidemiology of food allergy. Pediatr Clin N Am. ;58(2)–CrossRef Scholar

    • Irvine AD, McLean WH, Leung DY. Filaggrin mutations associated with skin and allergic diseases. N Engl J Med. ;(14)–CrossRef Scholar

    • 6.

      Liu AH, Jaramillo R, Sicherer SH, Wood RA, Bock SA, Burks AW, et al.

      National prevalence and risk factors for food allergy and relationship to asthma: results from the National Health and Nutrition Examination Survey – J Allergy Clin Immunol. ;(4)–CrossRef Scholar

    • Bager P, Wohlfahrt J, Westergaard T. Caesarean delivery and risk of atopy and allergic disesase: Meta-analyses. Clinical & Experimental Allergy 38 ():
    • Lack G, Fox D, Northstone K, et al. Factors associated with the development of peanut allergy in childhood. New England Journal of Medicine ():
    • Spergel JM, Paller AS. Atopic dermatitis and the atopic march. J Allergy Clin Immunol. ;(6 Suppl):S–CrossRef Scholar

    • 7.

      Arabkhazaeli A, Vijverberg SJ, van Erp FC, Raaijmakers JA, van der Ent CK, van der Maitland Zee AH.

      Characteristics and severity of asthma in children with and without atopic conditions: a cross-sectional study. BMC Pediatr. ;CrossRef Scholar

    • Woods RK, Thien F, Raven J, Walters EH, Abramson M. Prevalence of food allergies in young adults and their relationship to asthma, nasal allergies, and eczema. Ann Allergy Asthma Immunol. ;88(2)–ef Scholar

    • Tariq SM, Matthews SM, Hakim EA, Arshad SH. Egg allergy in infancy predicts respiratory allergic disease by 4 years of age. Pediatr Allergy Immunol. ;11(3)–ef Scholar

    • Ziyab AH, Karmaus W, Zhang H, Holloway JW, Steck SE, Ewart S, et al. Allergic sensitization and filaggrin variants predispose to the comorbidity of eczema, asthma, and rhinitis: results from the Isle of Wight birth cohort.

      Clin Exp Allergy. ;44(9)–ef Scholar

    • James JM, Eigenmann PA, Eggleston PA, Sampson HA. Airway reactivity changes in asthmatic patients undergoing blinded food challenges. Am J Respir Crit Care Med. ;(2)–CrossRef Scholar

    • Roberts G, Golder N, Lack G. Bronchial challenges with aerosolized food in asthmatic, food-allergic children. Allergy. ;57(8)–ef Scholar

    • Webber CM, England RW. Oral allergy syndrome: a clinical, diagnostic, and therapeutic challenge. Ann Allergy Asthma Immunol. ;(2)–8; quiz 9–10, CrossRef Scholar

    • Comstock SS, DeMera R, Vega LC, Boren EJ, Deane S, Haapanen LA, et al.

      Allergic reactions to peanuts, tree nuts, and seeds aboard commercial airliners. Ann Allergy Asthma Immunol. ;(1)–ef Scholar

    • Xu F, Yan S, Zheng Q, et al.

      What is the most common food allergy in uk

      Residential risk factors for atopic dermatitis in 3-to 6-year ancient children: A cross-sectional study in shanghai, china. International Journal of Environmental Research and Public Health ():

    • Melén E, Nyberg F, Lindgren CM, et al. Interactions between glutathione s-transferase p1, tumor necrosis factor, and traffic-related air pollution for development of childhood allergic disease. Environmental Health Perspectives ():
    • Young E, Stoneham MD, Petruckevitch A, et al.

      A population study of food intolerance. The Lancet ():

    • Liu X, Zhang S, Tsai HJ, et al. Genetic and environmental contributions to allergen sensitization in a chinese twin study. Clinical & Experimental Allergy 39 ():
    • 4.

      Savage J, Johns CB. Food allergy: epidemiology and natural history. Immunol Allergy Clin N Am. ;35(1)–CrossRef Scholar

    • Jackson KD, Howie LD, Akinbami LJ.

      Trends in allergic conditions among children: United states, (National Middle for Health Statistics Data Brief).National Middle for Health Statistics, Centers for Disease Control ().

    • Dotterud CK, Storrø O, Johnsen R, et al. Probiotics in pregnant women to prevent allergic disease: A randomized, double-blind trial. British Journal of Dermatology ():
    • Heyman MB. Lactose intolerance in infants, children, and adolescents. Pediatrics ():
    • Stefka AT, Feehley T, Tripathi P, et al. Commensal bacteria protect against food allergen sensitization. Proceedings of the National Academy of Sciences ():
    • 8.

      Illi S, von Mutius E, Lau S, Nickel R, Niggemann B, Sommerfeld C, et al.

      The pattern of atopic sensitization is associated with the development of asthma in childhood. J Allergy Clin Immunol. ;(5)–CrossRef Scholar

    • 2.

      Dahlman-Hoglund A, Renstrom A, Larsson PH, Elsayed S, Andersson E. Salmon allergen exposure, occupational asthma, and respiratory symptoms among salmon processing workers. Am J Ind Med. ;55(7)–CrossRef Scholar

    • Bao Y, Chen Z, Liu E, Xiang L, Zhao D, Hong J. Risk factors in preschool children for predicting asthma during the preschool age and the early school age: a systematic review and meta-analysis.

      Curr Allergy Asthma Rep. ;17(12)CrossRef Scholar

    • Teufel M, Biedermann T, Rapps N, et al. Psychological burden of food allergy. World Journal of Gastroenterology: WJG 13 ():
    • Best KP, Sullivan TR, Palmer DJ, Gold M, Martin J, Kennedy D, et al. Prenatal omega-3 LCPUFA and symptoms of allergic disease and sensitization throughout early childhood — a longitudinal analysis of long-term follow-up of a randomized controlled trial. World Allergy Organ J. ;11(1)CrossRef Scholar

    • Bergmann RL, Edenharter G, Bergmann KE, Forster J, Bauer CP, Wahn V, et al.

      Atopic dermatitis in early infancy predicts allergic airway disease at 5 years. Clin Exp Allergy. ;28(8)–CrossRef Scholar

    • Kemp AS. Epipen epidemic: Suggestions for rational prescribing in childhood food allergy. Journal of Paediatrics and Kid Health 39 ():
    • Christie L, Hine RJ, Parker JG, et al. Food allergies in children affect nutrient intake and growth. Journal of the American Dietetic Association ():
    • Dempfle A, Scherag A, Hein R, et al.

      Gene? environment interactions for complicated traits: Definitions, methodological requirements and challenges. European Journal of Human Genetics 16 ():

    • 3.

      Rona RJ, Keil T, Summers C, Gislason D, Zuidmeer L, Sodergren E, et al. The prevalence of food allergy: a meta-analysis. J Allergy Clin Immunol. ;(3)–CrossRef Scholar

    • Du Toit G, Roberts G, Sayre PH, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy.

      New England Journal Medicine ():

    • Ho MH-K, Wong WH-S, Chang C. Clinical spectrum of food allergies: A comprehensive review. Clinical reviews in allergy and immunology 46 ():
    • Cummings AJ, Knibb RC, King RM, et al. The psychosocial impact of food allergy and food hypersensitivity in children, adolescents and their families: A review. Allergy 65 ():
    • Bedolla-Barajas M, Kestler-Gramajo A, Alcalá-Padilla G, et al. Prevalence of oral allergy syndrome in children with allergic diseases. Allergologia et Immunopathologia 45 ():
    • Hill DJ, Firer MA, Shelton MJ, Hosking CS.

      Manifestations of milk allergy in infancy: clinical and immunologic findings. J Pediatr. ;(2)–ef Scholar

    • Farioli L, Losappio LM, Giuffrida MG, Pravettoni V, Micarelli G, Nichelatti M, et al. Mite-induced asthma and IgE levels to shrimp, mite, tropomyosin, arginine kinase, and Der p 10 are the most risk factors for challenge-provenshrimp allergy. Int Arch Allergy Immunol. ;(3–4)–CrossRef Scholar

    • Yepes-Nunez JJ, Brozek JL, Fiocchi A, Pawankar R, Cuello-Garcia C, Zhang Y, et al. Vitamin D supplementation in primary allergy prevention: Systematic systematic review of randomized and non-randomized studies. Allergy. ;73(1)–CrossRef Scholar

    • Roberts G, Lack G.

      Relevance of inhalational exposure to food allergens. Curr Opin Allergy Clin Immunol. ;3(3)–ef Scholar

    • Panel NIoAaID-SE. Guidelines for the diagnosis and management of food allergy in the United States: Report of the niaid-sponsored expert panel. (Journal of Allergy and Clinical Immunology). National Institute of Allergy and Infectious Diseases.
    • Mansfield LE. Oral immunotherapy for peanut allergy in clinical practice is ready. In: Proceedings of the Allergy and Asthma Proceedings. OceanSide Publications, Inc 34 ():
    • •• Pettersson ME, Koppelman GH, Flokstra-de Blok BMJ, Kollen BJ, Dubois AEJ.

      Prediction of the severity of allergic reactions to foods. Allergy. ;73(7)– This study underwrites that the severity of double blind placebo controlled food challenges remains largely unpredictable.CrossRef Scholar

    • 9.

      Wang J, Visness CM, Sampson HA. Food allergen sensitization in inner-city children with asthma. J Allergy Clin Immunol. ;(5)–CrossRef Scholar

    • Eggesbø M, Botten G, Stigum H, et al. Is delivery by cesarean section a risk factor for food allergy?

      Journal of Allergy and clinical Immunology ():

    • Kim JS, Nowak-W?grzyn A, Sicherer SH, et al. Dietary baked milk accelerates the resolution of cow’s milk allergy in children. Journal of Allergy and Clinical Immunology ():
    • Ortolani C, Pastorello EA. Food allergies and food intolerances. Best Practice and Research Clinical Gastroenterology 20 ():
    • Amlot PL, Kemeny DM, Zachary C, Parkes P, Lessof MH. Oral allergy syndrome (OAS): symptoms of IgE-mediated hypersensitivity to foods. Clin Allergy. ;17(1)–CrossRef Scholar

    • •• Perkin MR, Logan K, Tseng A, Raji B, Ayis S, Peacock J, et al.

      Randomized trial of introduction of allergenic foods in breast-fed infants. N Engl J Med. ;(18)– This is a RCT in young children in which they show that early introduction of peanut and egg at the age of 3 months results in a reduction of peanut and egg allergy at a later age.CrossRef Scholar

    • Wjst M. Another explanation for the low allergy rate in the rural alpine foothills. Clinical and Molecular Allergy 3 (): 7.
    • Campbell CP, Yates DH.

      Lupin allergy: a hidden killer at home, a menace at work; occupational disease due to lupin allergy. Clin Exp Allergy. ;40(10)–CrossRef Scholar

    • Flohr C, Perkin M, Logan K, Marrs T, Radulovic S, Campbell LE, et al. Atopic dermatitis and disease severity are the main risk factors for food sensitization in exclusively breastfed infants. J Invest Dermatol. ;(2)–CrossRef Scholar

    • Allan K, Kelly FJ, Devereux G. Antioxidants and allergic disease: A case of too little or too much? Clinical and Experimental Allergy 40 ():
    • Arshad SH, Tariq SM, Matthews S, et al. Sensitization to common allergens and its association with allergic disorders at age 4 years: A whole population birth cohort study.

      Pediatrics (): ee

    • Macpherson AJ, Harris NL. Interactions between commensal intestinal bacteria and the immune system. Nature Reviews Immunology 4 ():
    • Mills ENC, Mackie AR, Burney P, et al. The prevalence, cost and basis of food allergy across europe. Allergy 62 ():
    • Salvatori N, Reccardini F, Convento M, Purinan A, Colle R, De Carli S, et al. Asthma induced by inhalation of flour in adults with food allergy to wheat. Clin Exp Allergy. ;38(8)–CrossRef Scholar

    • Hourihane JO, Dean TP, Warner JO. Peanut allergy in relation to heredity, maternal diet, and other atopic diseases: results of a questionnaire survey, skin prick testing, and food challenges.

      BMJ. ;()–CrossRef Scholar

    • Sharief S, Jariwala S, Kumar J, et al. Vitamin d levels and food and environmental allergies in the united states: Results from the national health and nutrition examination survey Journal of Allergy and Clinical Immunology ():
    • Simpson A, John SL, Jury F, et al. Endotoxin exposure, cd14, and allergic disease: An interaction between genes and the environment. American Journal of Respiratory and Critical Care Medicine ():
    • Sicherer SH, Furlong TJ, Maes HH, Desnick RJ, Sampson HA, Gelb BD.

      Genetics of peanut allergy: a twin study. J Allergy Clin Immunol. ;(1 Pt 1)–ef Scholar

    • Branum AM, Lukacs S. Food allergy among us children: Trends in prevalence and hospitalizations:US Department of Health and Human Services, Centers for Disease Control and Prevention, National Middle for Health Statistics ().
    • Murray CS, Canoy D, Buchan I, et al. Body mass index in young children and allergic disease: Gender differences in a longitudinal study.

      Clinical & Experimental Allergy 41 ():

    • Corso LC, Wiesner PJ, Halverson PK, et al. Using the essential services as a foundation for performance measurement and assessment of local public health systems. Journal of Public Health Management and Practice 6 ():
    • Black PN, Sharpe S. Dietary fat and asthma: Is there a connection? European Respiratory Journal 10 ():
    • Round JL, Mazmanian SK. The gut microbiota shapes intestinal immune responses during health and disease.

      Nature Reviews Immunology 9 ():

    • 1.

      Lai CK, Beasley R, Crane J, Foliaki S, Shah J, Weiland S, et al. Global variation in the prevalence and severity of asthma symptoms: phase three of the International Study of Asthma and Allergies in Childhood (ISAAC). Thorax. ;64(6)–CrossRef Scholar

    • Kramer MS, Matush L, Vanilovich I, Platt R, Bogdanovich N, Sevkovskaya Z, et al. Effect of prolonged and exclusive breast feeding on risk of allergy and asthma: cluster randomised trial. BMJ. ;()CrossRef Scholar

    • Meyer R, Fleming C, Dominguez-Ortega G, Lindley K, Michaelis L, Thapar N, et al.

      Manifestations of food protein induced gastrointestinal allergies presenting to a single tertiary paediatric gastroenterology unit. World Allergy Organ J. ;6(1)CrossRef Scholar

    • Pumphrey RS, Roberts IS. Postmortem findings after fatal anaphylactic reactions. J Clin Pathol. ;53(4)–ef Scholar

    • Majowicz SE, Meyer SB, Kirkpatrick SI, et al. Food, health, and complexity: Towards a conceptual understanding to guide collaborative public health action. BMC Public Health 16 ():
    • Kilpelainen M, Terho EO, Helenius H, et al.

      Farm environment in childhood prevents the development of allergies. Clinical Experimental Allergy 30 ():

    • Marks GB, Mihrshahi S, Kemp AS, Tovey ER, Webb K, Almqvist C, et al. Prevention of asthma during the first 5 years of life: a randomized controlled trial. J Allergy Clin Immunol. ;(1)–CrossRef Scholar

    • Jansen JJN, Kardinaal AFM, Huijbers G, et al. Prevalence of food allergy and intolerance in the adult dutch population.

      Journal of Allergy and Clinical Immunology 93 ():

    • Makhija MM, Robison RG, Caruso D, et al. Patterns of allergen sensitization and self-reported allergic disease in parents of food allergic children. Annals of Allergy, Asthma & Immunology ():
    • Rhodes HL, Sporik R, Thomas P, Holgate ST, Cogswell JJ. Early life risk factors for adult asthma: a birth cohort study of subjects at risk. J Allergy Clin Immunol. ;(5)–ef Scholar

    • Tan THT, Ellis JA, Saffery R, et al.

      The role of genetics and environment in the rise of childhood food allergy. Clinical & Experimental Allergy 42 ():

    • van Ree R, Antonicelli L, Akkerdaas JH, Pajno GB, Barberio G, Corbetta L, et al. Asthma after consumption of snails in house-dust-mite-allergic patients: a case of IgE cross-reactivity. Allergy. ;51(6)–CrossRef Scholar

    • (FARE) FARE. Facts and statistics ().
    • Scurlock AM, Burks AW, Jones SM. Oral immunotherapy for food allergy. Current Allergy and Asthma Reports 9 ():
    • Guillet G, Guillet MH.

      Natural history of sensitizations in atopic dermatitis. A 3-year follow-up in children: food allergy and high risk of respiratory symptoms. Arch Dermatol.

      What is the most common food allergy in uk

      ;(2)–CrossRef Scholar

    • Leser C, Hartmann AL, Praml G, Wuthrich B. The «“egg-egg»” syndrome: occupational respiratory allergy to airborne egg proteins with consecutive ingestive egg allergy in the bakery and confectionery industry. J Investig Allergol Clin Immunol. ;11(2)–PubMed

    Figure 1: The progression of food allergy diagnosis. This figure shows the possible interactions a body can own to an allergen. The three stages are: no sensitivity to the food, food sensitivity, and food allergy.

    Figure 2: Steps to overcome sensitivity related illness.

    Figure 3: (A) Current hypothesized associations between food allergies and external factors and articles associated with them.

    (B) Greatest number of papers published from search databases used versus the food allergy hypothesis number.

  • 1.

    Lai CK, Beasley R, Crane J, Foliaki S, Shah J, Weiland S, et al. Global variation in the prevalence and severity of asthma symptoms: phase three of the International Study of Asthma and Allergies in Childhood (ISAAC). Thorax. ;64(6)–CrossRef Scholar

  • 2.

    Dahlman-Hoglund A, Renstrom A, Larsson PH, Elsayed S, Andersson E. Salmon allergen exposure, occupational asthma, and respiratory symptoms among salmon processing workers. Am J Ind Med. ;55(7)–CrossRef Scholar

  • 3.

    Rona RJ, Keil T, Summers C, Gislason D, Zuidmeer L, Sodergren E, et al.

    The prevalence of food allergy: a meta-analysis. J Allergy Clin Immunol. ;(3)–CrossRef Scholar

  • 4.

    Savage J, Johns CB. Food allergy: epidemiology and natural history. Immunol Allergy Clin N Am. ;35(1)–CrossRef Scholar

  • 5.

    Venter C, Arshad SH. Epidemiology of food allergy. Pediatr Clin N Am. ;58(2)–CrossRef Scholar

  • 6.

    Liu AH, Jaramillo R, Sicherer SH, Wood RA, Bock SA, Burks AW, et al.

    National prevalence and risk factors for food allergy and relationship to asthma: results from the National Health and Nutrition Examination Survey – J Allergy Clin Immunol. ;(4)–CrossRef Scholar

  • 7.

    Arabkhazaeli A, Vijverberg SJ, van Erp FC, Raaijmakers JA, van der Ent CK, van der Maitland Zee AH. Characteristics and severity of asthma in children with and without atopic conditions: a cross-sectional study. BMC Pediatr. ;CrossRef Scholar

  • 8.

    Illi S, von Mutius E, Lau S, Nickel R, Niggemann B, Sommerfeld C, et al. The pattern of atopic sensitization is associated with the development of asthma in childhood. J Allergy Clin Immunol. ;(5)–CrossRef Scholar

  • 9.

    Wang J, Visness CM, Sampson HA.

    Food allergen sensitization in inner-city children with asthma. J Allergy Clin Immunol. ;(5)–CrossRef Scholar

  • Schroeder A, Kumar R, Pongracic JA, Sullivan CL, Caruso DM, Costello J, et al. Food allergy is associated with an increased risk of asthma. Clin Exp Allergy. ;39(2)–CrossRef Scholar

  • Hill DA, Grundmeier RW, Ram G, Spergel JM. The epidemiologic characteristics of healthcare provider-diagnosed eczema, asthma, allergic rhinitis, and food allergy in children: a retrospective cohort study.

    BMC Pediatr. ;CrossRef Scholar

  • Roberts G, Lack G. Relevance of inhalational exposure to food allergens. Curr Opin Allergy Clin Immunol. ;3(3)–ef Scholar

  • Tariq SM, Matthews SM, Hakim EA, Arshad SH. Egg allergy in infancy predicts respiratory allergic disease by 4 years of age. Pediatr Allergy Immunol. ;11(3)–ef Scholar

  • Spergel JM, Paller AS. Atopic dermatitis and the atopic march. J Allergy Clin Immunol. ;(6 Suppl):S–CrossRef Scholar

  • Rhodes HL, Sporik R, Thomas P, Holgate ST, Cogswell JJ.

    Early life risk factors for adult asthma: a birth cohort study of subjects at risk. J Allergy Clin Immunol. ;(5)–ef Scholar

  • Meyer R, Fleming C, Dominguez-Ortega G, Lindley K, Michaelis L, Thapar N, et al. Manifestations of food protein induced gastrointestinal allergies presenting to a single tertiary paediatric gastroenterology unit. World Allergy Organ J. ;6(1)CrossRef Scholar

  • •• Tsakok T, Marrs T, Mohsin M, Baron S, du Toit G, Till S, et al. Does atopic dermatitis cause food allergy? A systematic review. J Allergy Clin Immunol. ;(4)–8. This paper comprises a systematic analysis and review out of 66 research studies.

    It was concluded that there is a strong association between atopic dermatitis, food sensitization and food allergy.CrossRef Scholar

  • Flohr C, Perkin M, Logan K, Marrs T, Radulovic S, Campbell LE, et al. Atopic dermatitis and disease severity are the main risk factors for food sensitization in exclusively breastfed infants. J Invest Dermatol. ;(2)–CrossRef Scholar

  • Guillet G, Guillet MH. Natural history of sensitizations in atopic dermatitis. A 3-year follow-up in children: food allergy and high risk of respiratory symptoms. Arch Dermatol. ;(2)–CrossRef Scholar

  • Lack G.

    Epidemiologic risks for food allergy. J Allergy Clin Immunol. ;(6)–ef Scholar

  • Abo-Zaid G, Sharpe RA, Fleming LE, Depledge M, Osborne NJ. Association of baby eczema with childhood and adult asthma: analysis of data from the birth cohort study. Int J Environ Res Public Health. ;15(7).CrossRef Scholar

  • Bergmann RL, Edenharter G, Bergmann KE, Forster J, Bauer CP, Wahn V, et al. Atopic dermatitis in early infancy predicts allergic airway disease at 5 years. Clin Exp Allergy. ;28(8)–CrossRef Scholar

  • Bao Y, Chen Z, Liu E, Xiang L, Zhao D, Hong J.

    Risk factors in preschool children for predicting asthma during the preschool age and the early school age: a systematic review and meta-analysis. Curr Allergy Asthma Rep. ;17(12)CrossRef Scholar

  • Hourihane JO, Dean TP, Warner JO. Peanut allergy in relation to heredity, maternal diet, and other atopic diseases: results of a questionnaire survey, skin prick testing, and food challenges. BMJ. ;()–CrossRef Scholar

  • Sicherer SH, Furlong TJ, Maes HH, Desnick RJ, Sampson HA, Gelb BD. Genetics of peanut allergy: a twin study. J Allergy Clin Immunol. ;(1 Pt 1)–ef Scholar

  • Irvine AD, McLean WH, Leung DY.

    Filaggrin mutations associated with skin and allergic diseases. N Engl J Med. ;(14)–CrossRef Scholar

  • Ziyab AH, Karmaus W, Zhang H, Holloway JW, Steck SE, Ewart S, et al. Allergic sensitization and filaggrin variants predispose to the comorbidity of eczema, asthma, and rhinitis: results from the Isle of Wight birth cohort. Clin Exp Allergy. ;44(9)–ef Scholar

  • Marks GB, Mihrshahi S, Kemp AS, Tovey ER, Webb K, Almqvist C, et al. Prevention of asthma during the first 5 years of life: a randomized controlled trial. J Allergy Clin Immunol. ;(1)–CrossRef Scholar

  • Woods RK, Thien F, Raven J, Walters EH, Abramson M.

    Prevalence of food allergies in young adults and their relationship to asthma, nasal allergies, and eczema. Ann Allergy Asthma Immunol. ;88(2)–ef Scholar

  • Best KP, Sullivan TR, Palmer DJ, Gold M, Martin J, Kennedy D, et al. Prenatal omega-3 LCPUFA and symptoms of allergic disease and sensitization throughout early childhood — a longitudinal analysis of long-term follow-up of a randomized controlled trial. World Allergy Organ J. ;11(1)CrossRef Scholar

  • Yepes-Nunez JJ, Brozek JL, Fiocchi A, Pawankar R, Cuello-Garcia C, Zhang Y, et al.

    Vitamin D supplementation in primary allergy prevention: Systematic systematic review of randomized and non-randomized studies. Allergy. ;73(1)–CrossRef Scholar

  • Kramer MS, Matush L, Vanilovich I, Platt R, Bogdanovich N, Sevkovskaya Z, et al. Effect of prolonged and exclusive breast feeding on risk of allergy and asthma: cluster randomised trial. BMJ. ;()CrossRef Scholar

  • Koplin JJ, Osborne NJ, Wake M, Martin PE, Gurrin LC, Robinson MN, et al. Can early introduction of egg prevent egg allergy in infants?

    A population-based study. J Allergy Clin Immunol. ;(4)–CrossRef Scholar

  • •• Perkin MR, Logan K, Tseng A, Raji B, Ayis S, Peacock J, et al. Randomized trial of introduction of allergenic foods in breast-fed infants. N Engl J Med. ;(18)– This is a RCT in young children in which they show that early introduction of peanut and egg at the age of 3 months results in a reduction of peanut and egg allergy at a later age.CrossRef Scholar

  • Calvani M, Cardinale F, Martelli A, Muraro A, Pucci N, Savino F, et al.

    Risk factors for severe pediatric food anaphylaxis in Italy. Pediatr Allergy Immunol. ;22(8)–ef Scholar

  • Summers CW, Pumphrey RS, Woods CN, McDowell G, Pemberton PW, Arkwright PD. Factors predicting anaphylaxis to peanuts and tree nuts in patients referred to a specialist middle. J Allergy Clin Immunol. ;(3)–ef Scholar

  • Pumphrey RS, Roberts IS. Postmortem findings after fatal anaphylactic reactions. J Clin Pathol. ;53(4)–ef Scholar

  • van Erp FC, Knulst AC, Kentie PA, Pasmans SG, van der Ent CK, Meijer Y.

    Can we predict severe reactions during peanut challenges in children? Pediatr Allergy Immunol. ;24(6)–CrossRef Scholar

  • •• Pettersson ME, Koppelman GH, Flokstra-de Blok BMJ, Kollen BJ, Dubois AEJ. Prediction of the severity of allergic reactions to foods. Allergy. ;73(7)– This study underwrites that the severity of double blind placebo controlled food challenges remains largely unpredictable.CrossRef Scholar

  • Hill DJ, Firer MA, Shelton MJ, Hosking CS.

    Manifestations of milk allergy in infancy: clinical and immunologic findings. J Pediatr. ;(2)–ef Scholar

  • Bock SA, Munoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. J Allergy Clin Immunol. ;(1)–ef Scholar

  • James JM, Eigenmann PA, Eggleston PA, Sampson HA. Airway reactivity changes in asthmatic patients undergoing blinded food challenges. Am J Respir Crit Care Med. ;(2)–CrossRef Scholar

  • • Krogulska A, Dynowski J, Jedrzejczyk M, Sardecka I, Malachowska B, Wasowska-Krolikowska K.

    The impact of food allergens on airway responsiveness in schoolchildren with asthma: A a DBPCFC study. Pediatr Pulmonol. ;51(8)– This study shows that food allergens may enhance non-specific bronchial hyperresponsiveness.CrossRef Scholar

  • Ortolani C, Ispano M, Pastorello E, Bigi A, Ansaloni R. The oral allergy syndrome. Ann Allergy. ;61(6 Pt 2)–PubMed Scholar

  • Tuft L, Blumstein G. Studies in food allergy — sensitization to unused fruits: clinical and experimental observations.

    J Allergy Ther. ;–ef Scholar

  • Webber CM, England RW. Oral allergy syndrome: a clinical, diagnostic, and therapeutic challenge. Ann Allergy Asthma Immunol. ;(2)–8; quiz 9–10, CrossRef Scholar

  • Amlot PL, Kemeny DM, Zachary C, Parkes P, Lessof MH. Oral allergy syndrome (OAS): symptoms of IgE-mediated hypersensitivity to foods. Clin Allergy. ;17(1)–CrossRef Scholar

  • van Ree R, Antonicelli L, Akkerdaas JH, Pajno GB, Barberio G, Corbetta L, et al. Asthma after consumption of snails in house-dust-mite-allergic patients: a case of IgE cross-reactivity.

    Allergy. ;51(6)–CrossRef Scholar

  • Farioli L, Losappio LM, Giuffrida MG, Pravettoni V, Micarelli G, Nichelatti M, et al. Mite-induced asthma and IgE levels to shrimp, mite, tropomyosin, arginine kinase, and Der p 10 are the most risk factors for challenge-provenshrimp allergy. Int Arch Allergy Immunol. ;(3–4)–CrossRef Scholar

  • Roberts G, Golder N, Lack G. Bronchial challenges with aerosolized food in asthmatic, food-allergic children.

    Allergy. ;57(8)–ef Scholar

  • Comstock SS, DeMera R, Vega LC, Boren EJ, Deane S, Haapanen LA, et al. Allergic reactions to peanuts, tree nuts, and seeds aboard commercial airliners. Ann Allergy Asthma Immunol. ;(1)–ef Scholar

  • •• Baur X. A compendium of causative agents of occupational asthma. J Occup Med Toxicol. ;8(1) A comprehensive overview of agents that may induce occupational asthma.CrossRef Scholar

  • Salvatori N, Reccardini F, Convento M, Purinan A, Colle R, De Carli S, et al. Asthma induced by inhalation of flour in adults with food allergy to wheat. Clin Exp Allergy. ;38(8)–CrossRef Scholar

  • Campbell CP, Yates DH.

    Lupin allergy: a hidden killer at home, a menace at work; occupational disease due to lupin allergy. Clin Exp Allergy. ;40(10)–CrossRef Scholar

  • Leser C, Hartmann AL, Praml G, Wuthrich B. The «“egg-egg»” syndrome: occupational respiratory allergy to airborne egg proteins with consecutive ingestive egg allergy in the bakery and confectionery industry. J Investig Allergol Clin Immunol. ;11(2)–PubMed

  • Observational studies

    Several observational studies own suggested that early introduction of potentially allergenic foods may be associated with a decreased risk of developing food allergy.

    A questionnaire-based survey conducted in found that the prevalence of peanut allergy was ten-fold higher among Jewish children in the United Kingdom (UK) compared with Jewish children in Israel [12]. This difference in prevalence was attributed to earlier and more frequent peanut exposure in the first year of life in Israel compared with the UK. A population-based, cross-sectional study (HealthNuts) that included over infants found a lower risk of egg allergy among those that were introduced to egg at 4–6 month of age compared to those introduced at 10–12 months of age or later [13].

    Another observational study examining the feeding history of over 13, infants found the incidence of IgE-mediated cow’s milk allergy to be significantly lower in infants who were introduced to cow’s milk formula within the first 14 days of life and given it regularly thereafter, compared to those who were introduced to the formula after 3 months of age [14]. Similarly, a case–control study that included approximately children showed that early introduction of cow’s milk formula was associated with a lower incidence of IgE-mediated cow’s milk allergy [15]. Data from a Finnish birth cohort that included children found that delaying the introduction of multiple foods, including oats (> 5 months) and wheat (> 6 months), was significantly associated with an increased risk of allergic sensitization to food and inhalant allergens [16].

    Another birth cohort study conducted in the United States (US) showed that introducing solid food or cow’s milk (complementary food) at less than 4 months of age was associated with a reduced risk of peanut allergy by age 2–3 years in children with a parental history of asthma or allergy [17]. A study that included approximately children observed that delaying initial exposure to cereal grains until 6 months of age may increase the risk of developing IgE-mediated wheat allergy [18]. More recently, data from over children included in the Canadian Healthy Baby Longitudinal Development (CHILD) birth cohort study showed that delaying the introduction of cow’s milk products, egg, and peanut beyond the first year of life significantly increased the odds of sensitization to these foods [19].

    Prospective clinical trials

    In recent years, randomized controlled trials own provided further support for the association between early food introduction and the prevention of food allergy.

    The most compelling evidence to date comes from the LEAP study, which randomized high-risk infants (defined as those with severe eczema and/or egg allergy) in the UK to either early (age 4–11 months) or delayed (avoidance until age 5 years) peanut introduction. The trial showed that the early and regular (3 times per week) consumption of peanut in these high-risk infants reduced the development of peanut allergy by 86% by 5 years of age [4].

    The Persistence of Oral Tolerance to Peanut extension of the LEAP study (LEAP-On) investigated whether participants who had consumed peanut in the primary trial would remain protected from peanut allergy after cessation of peanut consumption for 12 months [20]. This extension study found that the benefits of early peanut introduction persisted after 12 months of cessation of peanut consumption, supporting the concept that early peanut tolerance is not a transient phenomenon.

    In the Enquiring About Tolerance (EAT) trial, exclusively breastfed infants from the general population were randomized to either early (age 3 months) or standard (age 6 months) introduction of six allergenic foods (peanut, cooked egg, cow’s milk, sesame, whitefish, and wheat) [21].

    The EAT investigators hypothesized that early introduction of these allergenic foods would reduce the prevalence of food allergy by age 3 years. The intention-to-treat analysis revealed a 20% reduction in the prevalence of food allergy in the early introduction group that was not statistically significant, likely because of the high rate of non-adherence to the dietary protocol. However, in an adjusted per protocol analysis, significant reductions were seen in the rates of peanut and egg allergy in the early introduction group.

    Other prospective trials own investigated the effects of early egg introduction.

    In the Prevention of Egg Allergy with Tiny Quantity Intake (PETIT) trial, Japanese infants with eczema were randomly assigned to daily consumption of heated egg powder or placebo along with aggressive treatment of eczema [22]. The study found that randomization to heated egg powder at age 6 months significantly reduced the risk of egg allergy by 78% compared with avoidance until age 12 months. The trial was stopped early due to benefit. The Solids Timing for Allergy Research (STAR) randomized 86 high-risk infants with moderate-to-severe eczema to get pasteurized raw whole-egg powder or rice powder (placebo) at 4 months of age [23].

    At 8 months, both groups were introduced to whole cooked egg under medical supervision. At 1-year, there was a non-significant trend toward a lower rate of egg allergy in the group who received pasteurized raw egg powder at age 4 months vs. whole cooked egg at age 8 months. However, the trial was terminated early due to the high rate of allergic reactions in the egg-sensitized children randomized to early introduction at age 4 months. The Starting Time of Egg Protein (STEP) study, which included infants without eczema but with a family history of atopy, found that early introduction of pasteurized raw egg powder at age 4–6 months was associated with a non-significant trend toward a reduced risk of egg allergy compared to introduction at age 10 months [24].

    A per-protocol analysis found that significantly fewer children in the early introduction group had IgE-mediated egg allergy at 12 months of age.

    In the Beating Egg Allergy Trial (BEAT), infants who were SPT-negative to egg but who had a family history of atopy were randomized to get either pasteurized whole-egg powder or placebo at 4 months of age [25]. Subjects were treated until 8 months of age, at which time egg was introduced into the diet. At 1 year, egg sensitization was significantly lower in the treatment group compared with the placebo group. However, there was only a non-significant trend toward a reduced risk of developing egg allergy in the early introduction group.

    Findings from the Hen’s Egg Allergy Prevention (HEAP) study also call into question the safety of early pasteurized raw egg introduction [26]. This trial, which included infants from the general population, found no evidence that early introduction of pasteurized raw egg powder at age 4–6 months prevented either egg allergy or egg sensitization. Furthermore, among the children with baseline egg sensitization who were excluded from randomization but then challenged with egg separately (n = 23), two-thirds experienced an anaphylactic reaction upon this initial introduction.

    Although the results of egg allergy studies own been conflicting or inconclusive, a recent meta-analysis of randomized controlled trials investigating the timing of allergenic food introduction and the risk of developing food allergy found “moderate certainty” evidence (based on 5 trials, including children) that introducing egg between 4 and 6 months of age reduced the risk of egg allergy (relative risk [RR], ; p = ) [27], showing much better efficacy with using cooked as opposed to raw egg.

    This meta-analysis also found “moderate certainty” evidence (based on 2 trials [LEAP and EAT], patients) that peanut introduction between age 4–11 months reduced the risk of peanut allergy (RR, ; p = ).

    Food Allergy

    Posted: March

    Alessandro Fiocchi, MD and Vincenzo Fierro, MD
    The Bambino Gesù Children’s Research Hospital
    Rome, Holy See

    Introduction

    Approximately 50 million Americans experience a food allergy. Food allergies affect up to six percent (6%) of children and four percent (4%) of adults (ACAAI ).

    Food allergies can develop at any age, but typically appear first during infancy or childhood (ACAAI ). However, in some occasions, an individual can develop an allergy, and subsequent adverse effect, to a food they own previously eaten with no negative symptoms (ACAAI ). In a
    recent study released by the Middle for Disease Control (), it was reported that between the years of and , food allergies among children increased 50% (CDC ). The number of food allergies is increasing, but the cause is unknown. The rate of anaphylaxis reactions after exposure to food is increasing, as well [1]. Anaphylactic reactions can be deadly if not immediately treated; key signs are facial swelling and difficulty breathing cause is unknown [1].

    Little data is available that postulates the causes of food allergies.

    However, some hypotheses own emerged over the past 10 years. For instance, factors such as race, ethnicity, and genetics contribute to allergy development (ACAAI ). More recently, research efforts own shifted from genetic-centric to synergistic reasoning incorporating environmental factors. Another striking statistic emerging in the literature over the past 5 years is the overwhelmingly high rates of food allergy development among individuals residing in first world countries, as compared to individuals who live in third world countries [2]. It has been postulated that the highly variable environmental factors in an industrialized nation contributes to the increase in the onset of food allergy [3].

    Food allergy conditions are a complicated diagnosis; each individual is affected differently.

    It is also a hard area of epidemiological, toxicological, or medicinal research because numerous food allergies are self-reported without qualifying or quantifying metrics (such as pathology, symptom, or biomarker identification). To complicate the subject further, a food allergy can exist along a continuum (or spectrum). Figure 1 describes the spectrum of food disorder; an Individual can own ‘no sensitivity’, food ‘sensitivity’, and/or a food ‘allergy’ to a food product. A food allergy is generally regarded as the more severe diseased state and induces an exaggerated immune response. Lastly, the allergic reaction to a food can vary among inflicted individuals.

    Example conditions arising from a food allergy could range from itching skin to urticarial outbreak to gastrointestinal dysfunction to anaphylaxis (CDC ).

    Literature presents the possible correlation between the environment and an increase in allergies. While no literature has yet to prove causation, a few articles own proposed possible correlations. Within the environmental construct of food and food delivery, the individual’s culture often promotes specific allergic reactions; if a food is not eaten in the population, then tolerance to the food is never developed, thus can result in a food allergy. A few significant research studies published in the literature own postulated that environmental factors influence the onset of food allergies, but extremely few own collected empirical data suggesting causation.

    Without causations and known ways to prevent food allergies, the epidemic will continue to grow and continue to adversely affect millions of people. A country’s food system can present itself as a cause to an allergen being present in the country or not. The dual-allergen-exposure hypothesis hypothesizes that in countries where a food is not consumed, there is no environmental exposure, an allergy to that food will not happen [4].

    An example of this occurred in the United Kingdom. Prior to , kiwis had never been present or eaten in the UK. Since the ’s when the kiwi was introduced to the UK, the rate of kiwi allergies has grown significantly [4].

    Another possible hypothesis could be in countries where they avoid a certain food i.e. peanuts, the rates of peanut allergies tend to be higher. There’s a misunderstanding that by completely avoiding and not introducing an infant/child to the item, they won’t develop an allergy. However, we’ve seen in America that this proves the opposite.

    Consequently, countries such as in Africa and some Asian countries where peanuts are widely eaten and avoided, there are extremely low rates of peanut allergies [4]. Researchers know that the environment plays a role in the development of food allergies, but few own studies own found concrete evidence to support the role that the environment plays. Some possible roles the environment contributes to food allergies include: traffic pollution, animal exposure, farm environment, smoking, and air pollution. One study reviewed found that long-term exposure to traffic pollutions can increase allergy sensitization [3].

    The study looked at children. One possibility of this correlation could be the knowledge that exposure to traffic and air pollution can increase rates of asthma which therefore can increase the rates of food allergies. Another study looked at the effects of dog ownership on the development of atopy among infants. It found that households that had a dog, the infants residing in these houses, were less likely to develop atopic dermatitis. This could appear in the form of eczema. It found that these results only proved true with dogs though, cats were evaluated as well but found to own no effect on the development of atopy [5].

    Two studies indicated evidence that early exposure to a farm environment could lower the risk of a kid developing atopy in the future.

    One study found that living on a farm in the early years helped to lift rates of genotype CD Low CD14 levels are associated with an increased risk of developing atopic sensitization. This study showed that the farm environment contributed to higher rates of CD14 among infants therefore, the infants had a lower risk of developing atopy [6]. Another study on farm environment found that a farm environment was successful in preventing allergic rhinitis (hay fever) and allergic conjunctivitis (itching eyes), but not allergic dermatitis (eczema) [7]. Allergic rhinitis and allergic conjunctivitis do not lead to the development of food allergies.

    More research needs to be done on the protective factors of a farm environment and the development of food allergies.

    Air pollution can be another cause of developing food allergies. A study found that passive or athletic smoking could frolic a role in the sensitization to food allergens. Passive smoking is inhalation of second-hand smoke and athletic smoking is a person who smokes. The same study found that exposure to aeroallergens or air pollutants can cause higher rates of respiratory infections which in turn might frolic an significant role in the sensitization to food allergens as well [8].

    The purpose of this review is to examine environmental factors as a cause of food allergies.

    First, we attempted to identify environmental factors that contribute to the increasing prevalence of food allergies in the past two decades. Second, we summarized the role that physiological factors (such as genetics, gender, and age) own played in the development of food allergies. Third, we evaluated the importance of the 10 Essential Services of Public Health in food allergy causation. The objective of this paper is to define the role of the environment as it relates to food allergies. If environmental factors contribute to the onset of food allergies, then this epidemic could be labeled as an emerging public health issue.

    Discussion

    Individual allergens, their prevalence and diagnoses

    A relatively little quantity of foods are referred to as major food allergens, i.e.

    foods known to elucidate an allergic reaction in humans. These foods include milk, egg, tree nuts, peanuts, seafood, shellfish, soy, and wheat [16]. People can exhibit intolerance to other foods, such as lactose or sulfites; but the adverse reaction to humans after exposure is not described as life threatening.

    Nut allergies (peanut and tree nut) are the leading cause of anaphylaxis, either fatal or nonfatal, in the United States and the United Kingdom [16].

    Unlike other food allergens, peanuts are linked to a genetic susceptibility. The environmental and physiological precursors to the development of a peanut allergy include early onset of a soy allergy and eczema as an baby, respectfully [17]. In some studies, maternal diet plays a role in the development of a peanut allergy, but other studies own proven this relation untrue [17]. A peanut allergy is unique in that the reaction is chronic and sustained throughout an individual’s life [17].

    According to several studies, the prevalence of food allergies are significantly lower in developing countries than those in developed countries [18].

    However, individuals from developing countries who immigrate to modernized countries lose their protection to certain allergens [18]. The difference between the rates of food allergy onset between developed versus developing countries could be due to factors in the local environmental construct.

    It is hard to pinpoint the rates of allergy prevalence due to the common practice of self- diagnosis, rather than practitioner diagnosis. Allergies can range from a less complicated intolerance or sensitivity to more complicated anaphylaxis. Few studies own been capable to accurately report the prevalence of certain food allergens [19]; and precise diagnosis is directly related to prevalence.

    The most widely accepted method to qualitatively diagnose an allergy is through either a skin test or blood test. Skin allergy testing is a method for medical diagnosis of allergies designed to inflame a controlled irritation response [20]. Blood allergy tests measure the upregulation of immunoglobulin E (IgE, the antibody that triggers food allergy symptoms) to specific foods [21]. In an ideal setting, the test would also include a double-blind, placebo-controlled food challenge (DBPCFC) [22].

    More precise prevalence rates for food allergies can be gained with more DBPCFC reported studies.

    Commonality among children

    The onset of food allergies diagnosed among children in the United States own risen 50% since [23]. Not only own the rates of allergies increased in the past two decades, but the rates of morbidity associated with allergies own risen, as well. Jackson et al.

    [23] concludes that there is no clear understanding of the reasons for the rising incidence rates; however, the nature of the interaction between genetic and environmental factors requires more research [23].

    Allergy vs. Sensitivity

    Any allergy has the potential to triggers a life threatening immune response. A sensitivity (also referred to as an intolerance) is generally not life threatening, but does result from the inability to metabolize or digest a food completely [22, 25].

    The majority of studies that focus on food allergies tend to avoid the more mild and less complicated food intolerances or sensitivities [26]. There evidence to propose, however, that some food sensitivities can lead to food allergies over time [27] (Figure 2). Most food intolerances and sensitivities are associated with abdominal symptoms such as nausea, bloating, and pain [28]. However, they can also be associated with symptoms such as neurological dysfunction, psychological disturbances, fibromyalgia, and skin rash [29].

    Although there are currently no proven methods to overcome a diagnosed food allergy, there are known ways to overcome a sensitivity related food illness.

    The first step includes completely eliminating the food from the diet, avoidance of the trigger response. The second step includes biochemical restoration. This is the body repairing itself since it is no longer experiencing illness. The third and final step is elimination of bioaccumulated toxicant load. Since the body is no longer experiencing the food item, it is capable to finish rid itself of the toxicants. In some cases, the food at this point can start to be reintroduced to the diet in little amounts.

    The most common food sensitivities include complicated carbohydrates, histamines, and lactase. In carbohydrate intolerance, an essential enzyme is missing from the digestion processes, which causes the incomplete metabolism of fermentable carbohydrates (i.e.

    sugars and starches). In histamine intolerance, foods with large quantity of the chemical histamine (i.e. alcohol, bananas, avocados, or eggplants) cause itchy eyes or tongue, runny nose, or congestion due to a lack of the enzyme diamine oxidase (DAO). In lactose intolerance, the enzyme lactase, responsible for breaking below lactose or milk sugar, is missing and causes diarrhea, nausea, vomiting, abdominal cramps, and bloating [25].

    Known causes and pre-existing health conditions

    There is limited information on the known causes of food allergies. There own been numerous correlations found but only a few studies own proven causation.

    Asthma and eczema are known pre-existing health conditions that often lead to the development of food allergies [30, 31]. Generally accepted correlations are listed below:

    Figure 1: The progression of food allergy diagnosis. This figure shows the possible interactions a body can own to an allergen. The three stages are: no sensitivity to the food, food sensitivity, and food allergy.

    Figure 2: Steps to overcome sensitivity related illness.

    Figure 3: (A) Current hypothesized associations between food allergies and external factors and articles associated with them.

    (B) Greatest number of papers published from search databases used versus the food allergy hypothesis number.

  • 1.

    Lai CK, Beasley R, Crane J, Foliaki S, Shah J, Weiland S, et al. Global variation in the prevalence and severity of asthma symptoms: phase three of the International Study of Asthma and Allergies in Childhood (ISAAC). Thorax. ;64(6)–CrossRef Scholar

  • 2.

    Dahlman-Hoglund A, Renstrom A, Larsson PH, Elsayed S, Andersson E.

    Salmon allergen exposure, occupational asthma, and respiratory symptoms among salmon processing workers. Am J Ind Med. ;55(7)–CrossRef Scholar

  • 3.

    Rona RJ, Keil T, Summers C, Gislason D, Zuidmeer L, Sodergren E, et al. The prevalence of food allergy: a meta-analysis. J Allergy Clin Immunol. ;(3)–CrossRef Scholar

  • 4.

    Savage J, Johns CB. Food allergy: epidemiology and natural history. Immunol Allergy Clin N Am. ;35(1)–CrossRef Scholar

  • 5.

    Venter C, Arshad SH. Epidemiology of food allergy.

    Pediatr Clin N Am. ;58(2)–CrossRef Scholar

  • 6.

    Liu AH, Jaramillo R, Sicherer SH, Wood RA, Bock SA, Burks AW, et al. National prevalence and risk factors for food allergy and relationship to asthma: results from the National Health and Nutrition Examination Survey – J Allergy Clin Immunol. ;(4)–CrossRef Scholar

  • 7.

    Arabkhazaeli A, Vijverberg SJ, van Erp FC, Raaijmakers JA, van der Ent CK, van der Maitland Zee AH. Characteristics and severity of asthma in children with and without atopic conditions: a cross-sectional study.

    BMC Pediatr. ;CrossRef Scholar

  • 8.

    Illi S, von Mutius E, Lau S, Nickel R, Niggemann B, Sommerfeld C, et al. The pattern of atopic sensitization is associated with the development of asthma in childhood. J Allergy Clin Immunol. ;(5)–CrossRef Scholar

  • 9.

    Wang J, Visness CM, Sampson HA. Food allergen sensitization in inner-city children with asthma. J Allergy Clin Immunol. ;(5)–CrossRef Scholar

  • Schroeder A, Kumar R, Pongracic JA, Sullivan CL, Caruso DM, Costello J, et al.

    Food allergy is associated with an increased risk of asthma. Clin Exp Allergy. ;39(2)–CrossRef Scholar

  • Hill DA, Grundmeier RW, Ram G, Spergel JM. The epidemiologic characteristics of healthcare provider-diagnosed eczema, asthma, allergic rhinitis, and food allergy in children: a retrospective cohort study. BMC Pediatr. ;CrossRef Scholar

  • Roberts G, Lack G. Relevance of inhalational exposure to food allergens. Curr Opin Allergy Clin Immunol. ;3(3)–ef Scholar

  • Tariq SM, Matthews SM, Hakim EA, Arshad SH.

    Egg allergy in infancy predicts respiratory allergic disease by 4 years of age. Pediatr Allergy Immunol. ;11(3)–ef Scholar

  • Spergel JM, Paller AS. Atopic dermatitis and the atopic march. J Allergy Clin Immunol. ;(6 Suppl):S–CrossRef Scholar

  • Rhodes HL, Sporik R, Thomas P, Holgate ST, Cogswell JJ. Early life risk factors for adult asthma: a birth cohort study of subjects at risk.

    J Allergy Clin Immunol. ;(5)–ef Scholar

  • Meyer R, Fleming C, Dominguez-Ortega G, Lindley K, Michaelis L, Thapar N, et al. Manifestations of food protein induced gastrointestinal allergies presenting to a single tertiary paediatric gastroenterology unit. World Allergy Organ J. ;6(1)CrossRef Scholar

  • •• Tsakok T, Marrs T, Mohsin M, Baron S, du Toit G, Till S, et al. Does atopic dermatitis cause food allergy? A systematic review. J Allergy Clin Immunol.

    ;(4)–8. This paper comprises a systematic analysis and review out of 66 research studies. It was concluded that there is a strong association between atopic dermatitis, food sensitization and food allergy.CrossRef Scholar

  • Flohr C, Perkin M, Logan K, Marrs T, Radulovic S, Campbell LE, et al. Atopic dermatitis and disease severity are the main risk factors for food sensitization in exclusively breastfed infants. J Invest Dermatol.

    ;(2)–CrossRef Scholar

  • Guillet G, Guillet MH. Natural history of sensitizations in atopic dermatitis. A 3-year follow-up in children: food allergy and high risk of respiratory symptoms. Arch Dermatol. ;(2)–CrossRef Scholar

  • Lack G. Epidemiologic risks for food allergy. J Allergy Clin Immunol. ;(6)–ef Scholar

  • Abo-Zaid G, Sharpe RA, Fleming LE, Depledge M, Osborne NJ. Association of baby eczema with childhood and adult asthma: analysis of data from the birth cohort study.

    Int J Environ Res Public Health. ;15(7).CrossRef Scholar

  • Bergmann RL, Edenharter G, Bergmann KE, Forster J, Bauer CP, Wahn V, et al. Atopic dermatitis in early infancy predicts allergic airway disease at 5 years. Clin Exp Allergy. ;28(8)–CrossRef Scholar

  • Bao Y, Chen Z, Liu E, Xiang L, Zhao D, Hong J. Risk factors in preschool children for predicting asthma during the preschool age and the early school age: a systematic review and meta-analysis.

    Curr Allergy Asthma Rep. ;17(12)CrossRef Scholar

  • Hourihane JO, Dean TP, Warner JO. Peanut allergy in relation to heredity, maternal diet, and other atopic diseases: results of a questionnaire survey, skin prick testing, and food challenges. BMJ. ;()–CrossRef Scholar

  • Sicherer SH, Furlong TJ, Maes HH, Desnick RJ, Sampson HA, Gelb BD. Genetics of peanut allergy: a twin study.

    J Allergy Clin Immunol. ;(1 Pt 1)–ef Scholar

  • Irvine AD, McLean WH, Leung DY. Filaggrin mutations associated with skin and allergic diseases. N Engl J Med. ;(14)–CrossRef Scholar

  • Ziyab AH, Karmaus W, Zhang H, Holloway JW, Steck SE, Ewart S, et al. Allergic sensitization and filaggrin variants predispose to the comorbidity of eczema, asthma, and rhinitis: results from the Isle of Wight birth cohort. Clin Exp Allergy. ;44(9)–ef Scholar

  • Marks GB, Mihrshahi S, Kemp AS, Tovey ER, Webb K, Almqvist C, et al. Prevention of asthma during the first 5 years of life: a randomized controlled trial. J Allergy Clin Immunol.

    ;(1)–CrossRef Scholar

  • Woods RK, Thien F, Raven J, Walters EH, Abramson M. Prevalence of food allergies in young adults and their relationship to asthma, nasal allergies, and eczema. Ann Allergy Asthma Immunol. ;88(2)–ef Scholar

  • Best KP, Sullivan TR, Palmer DJ, Gold M, Martin J, Kennedy D, et al. Prenatal omega-3 LCPUFA and symptoms of allergic disease and sensitization throughout early childhood — a longitudinal analysis of long-term follow-up of a randomized controlled trial. World Allergy Organ J. ;11(1)CrossRef Scholar

  • Yepes-Nunez JJ, Brozek JL, Fiocchi A, Pawankar R, Cuello-Garcia C, Zhang Y, et al. Vitamin D supplementation in primary allergy prevention: Systematic systematic review of randomized and non-randomized studies.

    Allergy. ;73(1)–CrossRef Scholar

  • Kramer MS, Matush L, Vanilovich I, Platt R, Bogdanovich N, Sevkovskaya Z, et al. Effect of prolonged and exclusive breast feeding on risk of allergy and asthma: cluster randomised trial. BMJ. ;()CrossRef Scholar

  • Koplin JJ, Osborne NJ, Wake M, Martin PE, Gurrin LC, Robinson MN, et al. Can early introduction of egg prevent egg allergy in infants? A population-based study. J Allergy Clin Immunol. ;(4)–CrossRef Scholar

  • •• Perkin MR, Logan K, Tseng A, Raji B, Ayis S, Peacock J, et al.

    Randomized trial of introduction of allergenic foods in breast-fed infants. N Engl J Med. ;(18)– This is a RCT in young children in which they show that early introduction of peanut and egg at the age of 3 months results in a reduction of peanut and egg allergy at a later age.CrossRef Scholar

  • Calvani M, Cardinale F, Martelli A, Muraro A, Pucci N, Savino F, et al. Risk factors for severe pediatric food anaphylaxis in Italy. Pediatr Allergy Immunol.

    ;22(8)–ef Scholar

  • Summers CW, Pumphrey RS, Woods CN, McDowell G, Pemberton PW, Arkwright PD. Factors predicting anaphylaxis to peanuts and tree nuts in patients referred to a specialist middle. J Allergy Clin Immunol. ;(3)–ef Scholar

  • Pumphrey RS, Roberts IS. Postmortem findings after fatal anaphylactic reactions. J Clin Pathol. ;53(4)–ef Scholar

  • van Erp FC, Knulst AC, Kentie PA, Pasmans SG, van der Ent CK, Meijer Y. Can we predict severe reactions during peanut challenges in children?

    Pediatr Allergy Immunol. ;24(6)–CrossRef Scholar

  • •• Pettersson ME, Koppelman GH, Flokstra-de Blok BMJ, Kollen BJ, Dubois AEJ. Prediction of the severity of allergic reactions to foods. Allergy. ;73(7)– This study underwrites that the severity of double blind placebo controlled food challenges remains largely unpredictable.CrossRef Scholar

  • Hill DJ, Firer MA, Shelton MJ, Hosking CS. Manifestations of milk allergy in infancy: clinical and immunologic findings.

    J Pediatr. ;(2)–ef Scholar

  • Bock SA, Munoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. J Allergy Clin Immunol. ;(1)–ef Scholar

  • James JM, Eigenmann PA, Eggleston PA, Sampson HA. Airway reactivity changes in asthmatic patients undergoing blinded food challenges. Am J Respir Crit Care Med. ;(2)–CrossRef Scholar

  • • Krogulska A, Dynowski J, Jedrzejczyk M, Sardecka I, Malachowska B, Wasowska-Krolikowska K. The impact of food allergens on airway responsiveness in schoolchildren with asthma: A a DBPCFC study.

    Pediatr Pulmonol. ;51(8)– This study shows that food allergens may enhance non-specific bronchial hyperresponsiveness.CrossRef Scholar

  • Ortolani C, Ispano M, Pastorello E, Bigi A, Ansaloni R. The oral allergy syndrome. Ann Allergy. ;61(6 Pt 2)–PubMed Scholar

  • Tuft L, Blumstein G. Studies in food allergy — sensitization to unused fruits: clinical and experimental observations. J Allergy Ther. ;–ef Scholar

  • Webber CM, England RW. Oral allergy syndrome: a clinical, diagnostic, and therapeutic challenge. Ann Allergy Asthma Immunol.

    ;(2)–8; quiz 9–10, CrossRef Scholar

  • Amlot PL, Kemeny DM, Zachary C, Parkes P, Lessof MH. Oral allergy syndrome (OAS): symptoms of IgE-mediated hypersensitivity to foods. Clin Allergy. ;17(1)–CrossRef Scholar

  • van Ree R, Antonicelli L, Akkerdaas JH, Pajno GB, Barberio G, Corbetta L, et al. Asthma after consumption of snails in house-dust-mite-allergic patients: a case of IgE cross-reactivity.

    Allergy. ;51(6)–CrossRef Scholar

  • Farioli L, Losappio LM, Giuffrida MG, Pravettoni V, Micarelli G, Nichelatti M, et al. Mite-induced asthma and IgE levels to shrimp, mite, tropomyosin, arginine kinase, and Der p 10 are the most risk factors for challenge-provenshrimp allergy. Int Arch Allergy Immunol. ;(3–4)–CrossRef Scholar

  • Roberts G, Golder N, Lack G. Bronchial challenges with aerosolized food in asthmatic, food-allergic children. Allergy. ;57(8)–ef Scholar

  • Comstock SS, DeMera R, Vega LC, Boren EJ, Deane S, Haapanen LA, et al.

    Allergic reactions to peanuts, tree nuts, and seeds aboard commercial airliners. Ann Allergy Asthma Immunol. ;(1)–ef Scholar

  • •• Baur X. A compendium of causative agents of occupational asthma. J Occup Med Toxicol. ;8(1) A comprehensive overview of agents that may induce occupational asthma.CrossRef Scholar

  • Salvatori N, Reccardini F, Convento M, Purinan A, Colle R, De Carli S, et al. Asthma induced by inhalation of flour in adults with food allergy to wheat.

    Clin Exp Allergy. ;38(8)–CrossRef Scholar

  • Campbell CP, Yates DH. Lupin allergy: a hidden killer at home, a menace at work; occupational disease due to lupin allergy. Clin Exp Allergy. ;40(10)–CrossRef Scholar

  • Leser C, Hartmann AL, Praml G, Wuthrich B. The «“egg-egg»” syndrome: occupational respiratory allergy to airborne egg proteins with consecutive ingestive egg allergy in the bakery and confectionery industry. J Investig Allergol Clin Immunol.

    ;11(2)–PubMed

  • Observational studies

    Several observational studies own suggested that early introduction of potentially allergenic foods may be associated with a decreased risk of developing food allergy. A questionnaire-based survey conducted in found that the prevalence of peanut allergy was ten-fold higher among Jewish children in the United Kingdom (UK) compared with Jewish children in Israel [12]. This difference in prevalence was attributed to earlier and more frequent peanut exposure in the first year of life in Israel compared with the UK. A population-based, cross-sectional study (HealthNuts) that included over infants found a lower risk of egg allergy among those that were introduced to egg at 4–6 month of age compared to those introduced at 10–12 months of age or later [13].

    Another observational study examining the feeding history of over 13, infants found the incidence of IgE-mediated cow’s milk allergy to be significantly lower in infants who were introduced to cow’s milk formula within the first 14 days of life and given it regularly thereafter, compared to those who were introduced to the formula after 3 months of age [14]. Similarly, a case–control study that included approximately children showed that early introduction of cow’s milk formula was associated with a lower incidence of IgE-mediated cow’s milk allergy [15]. Data from a Finnish birth cohort that included children found that delaying the introduction of multiple foods, including oats (> 5 months) and wheat (> 6 months), was significantly associated with an increased risk of allergic sensitization to food and inhalant allergens [16].

    Another birth cohort study conducted in the United States (US) showed that introducing solid food or cow’s milk (complementary food) at less than 4 months of age was associated with a reduced risk of peanut allergy by age 2–3 years in children with a parental history of asthma or allergy [17]. A study that included approximately children observed that delaying initial exposure to cereal grains until 6 months of age may increase the risk of developing IgE-mediated wheat allergy [18]. More recently, data from over children included in the Canadian Healthy Baby Longitudinal Development (CHILD) birth cohort study showed that delaying the introduction of cow’s milk products, egg, and peanut beyond the first year of life significantly increased the odds of sensitization to these foods [19].

    Prospective clinical trials

    In recent years, randomized controlled trials own provided further support for the association between early food introduction and the prevention of food allergy.

    The most compelling evidence to date comes from the LEAP study, which randomized high-risk infants (defined as those with severe eczema and/or egg allergy) in the UK to either early (age 4–11 months) or delayed (avoidance until age 5 years) peanut introduction. The trial showed that the early and regular (3 times per week) consumption of peanut in these high-risk infants reduced the development of peanut allergy by 86% by 5 years of age [4]. The Persistence of Oral Tolerance to Peanut extension of the LEAP study (LEAP-On) investigated whether participants who had consumed peanut in the primary trial would remain protected from peanut allergy after cessation of peanut consumption for 12 months [20].

    This extension study found that the benefits of early peanut introduction persisted after 12 months of cessation of peanut consumption, supporting the concept that early peanut tolerance is not a transient phenomenon.

    In the Enquiring About Tolerance (EAT) trial, exclusively breastfed infants from the general population were randomized to either early (age 3 months) or standard (age 6 months) introduction of six allergenic foods (peanut, cooked egg, cow’s milk, sesame, whitefish, and wheat) [21].

    The EAT investigators hypothesized that early introduction of these allergenic foods would reduce the prevalence of food allergy by age 3 years. The intention-to-treat analysis revealed a 20% reduction in the prevalence of food allergy in the early introduction group that was not statistically significant, likely because of the high rate of non-adherence to the dietary protocol. However, in an adjusted per protocol analysis, significant reductions were seen in the rates of peanut and egg allergy in the early introduction group.

    Other prospective trials own investigated the effects of early egg introduction.

    In the Prevention of Egg Allergy with Tiny Quantity Intake (PETIT) trial, Japanese infants with eczema were randomly assigned to daily consumption of heated egg powder or placebo along with aggressive treatment of eczema [22]. The study found that randomization to heated egg powder at age 6 months significantly reduced the risk of egg allergy by 78% compared with avoidance until age 12 months. The trial was stopped early due to benefit.

    The Solids Timing for Allergy Research (STAR) randomized 86 high-risk infants with moderate-to-severe eczema to get pasteurized raw whole-egg powder or rice powder (placebo) at 4 months of age [23]. At 8 months, both groups were introduced to whole cooked egg under medical supervision. At 1-year, there was a non-significant trend toward a lower rate of egg allergy in the group who received pasteurized raw egg powder at age 4 months vs. whole cooked egg at age 8 months. However, the trial was terminated early due to the high rate of allergic reactions in the egg-sensitized children randomized to early introduction at age 4 months.

    The Starting Time of Egg Protein (STEP) study, which included infants without eczema but with a family history of atopy, found that early introduction of pasteurized raw egg powder at age 4–6 months was associated with a non-significant trend toward a reduced risk of egg allergy compared to introduction at age 10 months [24]. A per-protocol analysis found that significantly fewer children in the early introduction group had IgE-mediated egg allergy at 12 months of age.

    In the Beating Egg Allergy Trial (BEAT), infants who were SPT-negative to egg but who had a family history of atopy were randomized to get either pasteurized whole-egg powder or placebo at 4 months of age [25].

    Subjects were treated until 8 months of age, at which time egg was introduced into the diet. At 1 year, egg sensitization was significantly lower in the treatment group compared with the placebo group. However, there was only a non-significant trend toward a reduced risk of developing egg allergy in the early introduction group. Findings from the Hen’s Egg Allergy Prevention (HEAP) study also call into question the safety of early pasteurized raw egg introduction [26].

    This trial, which included infants from the general population, found no evidence that early introduction of pasteurized raw egg powder at age 4–6 months prevented either egg allergy or egg sensitization. Furthermore, among the children with baseline egg sensitization who were excluded from randomization but then challenged with egg separately (n = 23), two-thirds experienced an anaphylactic reaction upon this initial introduction.

    Although the results of egg allergy studies own been conflicting or inconclusive, a recent meta-analysis of randomized controlled trials investigating the timing of allergenic food introduction and the risk of developing food allergy found “moderate certainty” evidence (based on 5 trials, including children) that introducing egg between 4 and 6 months of age reduced the risk of egg allergy (relative risk [RR], ; p = ) [27], showing much better efficacy with using cooked as opposed to raw egg.

    This meta-analysis also found “moderate certainty” evidence (based on 2 trials [LEAP and EAT], patients) that peanut introduction between age 4–11 months reduced the risk of peanut allergy (RR, ; p = ).

    Food Allergy

    Posted: March

    Alessandro Fiocchi, MD and Vincenzo Fierro, MD
    The Bambino Gesù Children’s Research Hospital
    Rome, Holy See

    Introduction

    Approximately 50 million Americans experience a food allergy. Food allergies affect up to six percent (6%) of children and four percent (4%) of adults (ACAAI ). Food allergies can develop at any age, but typically appear first during infancy or childhood (ACAAI ).

    However, in some occasions, an individual can develop an allergy, and subsequent adverse effect, to a food they own previously eaten with no negative symptoms (ACAAI ). In a
    recent study released by the Middle for Disease Control (), it was reported that between the years of and , food allergies among children increased 50% (CDC ). The number of food allergies is increasing, but the cause is unknown. The rate of anaphylaxis reactions after exposure to food is increasing, as well [1]. Anaphylactic reactions can be deadly if not immediately treated; key signs are facial swelling and difficulty breathing cause is unknown [1].

    Little data is available that postulates the causes of food allergies.

    However, some hypotheses own emerged over the past 10 years. For instance, factors such as race, ethnicity, and genetics contribute to allergy development (ACAAI ). More recently, research efforts own shifted from genetic-centric to synergistic reasoning incorporating environmental factors. Another striking statistic emerging in the literature over the past 5 years is the overwhelmingly high rates of food allergy development among individuals residing in first world countries, as compared to individuals who live in third world countries [2].

    It has been postulated that the highly variable environmental factors in an industrialized nation contributes to the increase in the onset of food allergy [3].

    Food allergy conditions are a complicated diagnosis; each individual is affected differently. It is also a hard area of epidemiological, toxicological, or medicinal research because numerous food allergies are self-reported without qualifying or quantifying metrics (such as pathology, symptom, or biomarker identification). To complicate the subject further, a food allergy can exist along a continuum (or spectrum). Figure 1 describes the spectrum of food disorder; an Individual can own ‘no sensitivity’, food ‘sensitivity’, and/or a food ‘allergy’ to a food product.

    A food allergy is generally regarded as the more severe diseased state and induces an exaggerated immune response. Lastly, the allergic reaction to a food can vary among inflicted individuals. Example conditions arising from a food allergy could range from itching skin to urticarial outbreak to gastrointestinal dysfunction to anaphylaxis (CDC ).

    Literature presents the possible correlation between the environment and an increase in allergies. While no literature has yet to prove causation, a few articles own proposed possible correlations. Within the environmental construct of food and food delivery, the individual’s culture often promotes specific allergic reactions; if a food is not eaten in the population, then tolerance to the food is never developed, thus can result in a food allergy.

    A few significant research studies published in the literature own postulated that environmental factors influence the onset of food allergies, but extremely few own collected empirical data suggesting causation. Without causations and known ways to prevent food allergies, the epidemic will continue to grow and continue to adversely affect millions of people. A country’s food system can present itself as a cause to an allergen being present in the country or not. The dual-allergen-exposure hypothesis hypothesizes that in countries where a food is not consumed, there is no environmental exposure, an allergy to that food will not happen [4].

    An example of this occurred in the United Kingdom. Prior to , kiwis had never been present or eaten in the UK. Since the ’s when the kiwi was introduced to the UK, the rate of kiwi allergies has grown significantly [4].

    Another possible hypothesis could be in countries where they avoid a certain food i.e. peanuts, the rates of peanut allergies tend to be higher. There’s a misunderstanding that by completely avoiding and not introducing an infant/child to the item, they won’t develop an allergy.

    However, we’ve seen in America that this proves the opposite. Consequently, countries such as in Africa and some Asian countries where peanuts are widely eaten and avoided, there are extremely low rates of peanut allergies [4]. Researchers know that the environment plays a role in the development of food allergies, but few own studies own found concrete evidence to support the role that the environment plays. Some possible roles the environment contributes to food allergies include: traffic pollution, animal exposure, farm environment, smoking, and air pollution. One study reviewed found that long-term exposure to traffic pollutions can increase allergy sensitization [3].

    The study looked at children. One possibility of this correlation could be the knowledge that exposure to traffic and air pollution can increase rates of asthma which therefore can increase the rates of food allergies. Another study looked at the effects of dog ownership on the development of atopy among infants. It found that households that had a dog, the infants residing in these houses, were less likely to develop atopic dermatitis. This could appear in the form of eczema.

    It found that these results only proved true with dogs though, cats were evaluated as well but found to own no effect on the development of atopy [5].

    Two studies indicated evidence that early exposure to a farm environment could lower the risk of a kid developing atopy in the future. One study found that living on a farm in the early years helped to lift rates of genotype CD Low CD14 levels are associated with an increased risk of developing atopic sensitization. This study showed that the farm environment contributed to higher rates of CD14 among infants therefore, the infants had a lower risk of developing atopy [6].

    Another study on farm environment found that a farm environment was successful in preventing allergic rhinitis (hay fever) and allergic conjunctivitis (itching eyes), but not allergic dermatitis (eczema) [7]. Allergic rhinitis and allergic conjunctivitis do not lead to the development of food allergies. More research needs to be done on the protective factors of a farm environment and the development of food allergies.

    Air pollution can be another cause of developing food allergies. A study found that passive or athletic smoking could frolic a role in the sensitization to food allergens.

    Passive smoking is inhalation of second-hand smoke and athletic smoking is a person who smokes. The same study found that exposure to aeroallergens or air pollutants can cause higher rates of respiratory infections which in turn might frolic an significant role in the sensitization to food allergens as well [8].

    The purpose of this review is to examine environmental factors as a cause of food allergies. First, we attempted to identify environmental factors that contribute to the increasing prevalence of food allergies in the past two decades.

    Second, we summarized the role that physiological factors (such as genetics, gender, and age) own played in the development of food allergies. Third, we evaluated the importance of the 10 Essential Services of Public Health in food allergy causation. The objective of this paper is to define the role of the environment as it relates to food allergies. If environmental factors contribute to the onset of food allergies, then this epidemic could be labeled as an emerging public health issue.

    Discussion

    Individual allergens, their prevalence and diagnoses

    A relatively little quantity of foods are referred to as major food allergens, i.e.

    foods known to elucidate an allergic reaction in humans. These foods include milk, egg, tree nuts, peanuts, seafood, shellfish, soy, and wheat [16]. People can exhibit intolerance to other foods, such as lactose or sulfites; but the adverse reaction to humans after exposure is not described as life threatening.

    Nut allergies (peanut and tree nut) are the leading cause of anaphylaxis, either fatal or nonfatal, in the United States and the United Kingdom [16].

    Unlike other food allergens, peanuts are linked to a genetic susceptibility. The environmental and physiological precursors to the development of a peanut allergy include early onset of a soy allergy and eczema as an baby, respectfully [17]. In some studies, maternal diet plays a role in the development of a peanut allergy, but other studies own proven this relation untrue [17]. A peanut allergy is unique in that the reaction is chronic and sustained throughout an individual’s life [17].

    According to several studies, the prevalence of food allergies are significantly lower in developing countries than those in developed countries [18].

    However, individuals from developing countries who immigrate to modernized countries lose their protection to certain allergens [18]. The difference between the rates of food allergy onset between developed versus developing countries could be due to factors in the local environmental construct.

    It is hard to pinpoint the rates of allergy prevalence due to the common practice of self- diagnosis, rather than practitioner diagnosis. Allergies can range from a less complicated intolerance or sensitivity to more complicated anaphylaxis. Few studies own been capable to accurately report the prevalence of certain food allergens [19]; and precise diagnosis is directly related to prevalence.

    The most widely accepted method to qualitatively diagnose an allergy is through either a skin test or blood test. Skin allergy testing is a method for medical diagnosis of allergies designed to inflame a controlled irritation response [20]. Blood allergy tests measure the upregulation of immunoglobulin E (IgE, the antibody that triggers food allergy symptoms) to specific foods [21]. In an ideal setting, the test would also include a double-blind, placebo-controlled food challenge (DBPCFC) [22]. More precise prevalence rates for food allergies can be gained with more DBPCFC reported studies.

    Commonality among children

    The onset of food allergies diagnosed among children in the United States own risen 50% since [23].

    Not only own the rates of allergies increased in the past two decades, but the rates of morbidity associated with allergies own risen, as well. Jackson et al. [23] concludes that there is no clear understanding of the reasons for the rising incidence rates; however, the nature of the interaction between genetic and environmental factors requires more research [23].

    Allergy vs. Sensitivity

    Any allergy has the potential to triggers a life threatening immune response. A sensitivity (also referred to as an intolerance) is generally not life threatening, but does result from the inability to metabolize or digest a food completely [22, 25].

    The majority of studies that focus on food allergies tend to avoid the more mild and less complicated food intolerances or sensitivities [26]. There evidence to propose, however, that some food sensitivities can lead to food allergies over time [27] (Figure 2). Most food intolerances and sensitivities are associated with abdominal symptoms such as nausea, bloating, and pain [28]. However, they can also be associated with symptoms such as neurological dysfunction, psychological disturbances, fibromyalgia, and skin rash [29].

    Although there are currently no proven methods to overcome a diagnosed food allergy, there are known ways to overcome a sensitivity related food illness.

    The first step includes completely eliminating the food from the diet, avoidance of the trigger response. The second step includes biochemical restoration. This is the body repairing itself since it is no longer experiencing illness. The third and final step is elimination of bioaccumulated toxicant load. Since the body is no longer experiencing the food item, it is capable to finish rid itself of the toxicants. In some cases, the food at this point can start to be reintroduced to the diet in little amounts.

    The most common food sensitivities include complicated carbohydrates, histamines, and lactase. In carbohydrate intolerance, an essential enzyme is missing from the digestion processes, which causes the incomplete metabolism of fermentable carbohydrates (i.e.

    sugars and starches). In histamine intolerance, foods with large quantity of the chemical histamine (i.e. alcohol, bananas, avocados, or eggplants) cause itchy eyes or tongue, runny nose, or congestion due to a lack of the enzyme diamine oxidase (DAO). In lactose intolerance, the enzyme lactase, responsible for breaking below lactose or milk sugar, is missing and causes diarrhea, nausea, vomiting, abdominal cramps, and bloating [25].

    Known causes and pre-existing health conditions

    There is limited information on the known causes of food allergies.

    There own been numerous correlations found but only a few studies own proven causation. Asthma and eczema are known pre-existing health conditions that often lead to the development of food allergies [30, 31]. Generally accepted correlations are listed below:

    • Children tend to own more than one food allergy present at a time [17].
    • Eczema in infants is an early indicator to the presence of a food allergy [32].
    • Individuals with asthma tend to own a food allergy [16].
    • Genetic history of food allergies can increase the risk for developing a food allergy tenfold [16, 21].

    A few relationships between environmental factors and food allergies that own been studied but are inconclusive and often debated:

    A few relationships between environmental factors and food allergies that own been studied but are inconclusive and often debated:

    • Some foods prepared and eaten raw (uncooked) induce adverse allergic reactions; however, some of the same foods prepared and eaten cooked also induce the same reaction [34].
    • Antibiotic use in children, as well as lack of healthy commensal bacteria has shown to be a risk factor for developing food allergies; but, the trends in observed data are not general [35].
    • “hypersensitivity” is defined as “conditions clinically resembling allergy that cause objectively reproducible symptoms or signs, initiated by exposure to a defined stimulus at a dose tolerated by normal subjects”, and
    • A higher body mass index (BMI) is associated with an increased risk of allergies in children; however, the association varies depending on gender, age, and type of allergen [33].
    • the term “atopy” is used when individuals own an IgE sensitization as documented by IgE antibodies in serum or by a positive skin prick test;
    • “allergy” is defined “a hypersensitivity reaction initiated by proven or strongly suspected immunologic mechanisms”.

    Competing Financial Interests Declaration

    Neither ENB nor CMS own any conflicts of interest, financial or otherwise.

    Competing Financial Interests Declaration

    Neither ENB nor CMS own any conflicts of interest, financial or otherwise.

    Definition and Classification

    The classification of allergic and hypersensitivity diseases was established by the European Academy of Allergy and Clinical Immunology (EAACI) and the World Allergy Organization (WAO) in (1).

    The definitions and concepts of allergic and hypersensitivity conditions beyond the allergy community own often created misunderstanding (2). For an optimal clarification:

    1. the term “atopy” is used when individuals own an IgE sensitization as documented by IgE antibodies in serum or by a positive skin prick test;
    2. “hypersensitivity” is defined as “conditions clinically resembling allergy that cause objectively reproducible symptoms or signs, initiated by exposure to a defined stimulus at a dose tolerated by normal subjects”, and
    3. “allergy” is defined “a hypersensitivity reaction initiated by proven or strongly suspected immunologic mechanisms”.

    Based on these definitions, a correct diagnosis of allergic disease must adhere to the following conditions:

    a) Compatible clinical history; and
    b) Positivity to in vivo and/or in vitro tests to prove underlying mechanism and etiology.

    The tests alone cannot be used because numerous people are sensitized (positive results to in vivo and/or in vitro tests), but not allergic (no reactions).

    Specifically for ‘food allergy’, this term is used when a causal relationship (ideally, with a specific immunological mechanism) has been defined.

    There are three wide groups of immune reactions: IgE-mediated, non-IgE-mediated and mixed. The IgE-mediated reactions are generally divided into immediate-onset reactions (arising up to 2 hours from the food ingestion) and immediate plus late-phase (in which the immediate onset symptoms are followed by prolonged or ongoing symptoms). Non-IgE-mediated reactions, which are poorly defined both clinically and scientifically, are believed to be generally T-cell-mediated. They are typically delayed in onset, and happen 4 to 28 hours after ingestion of the offending food(s). Mixed IgE and non-IgE mediated reaction are conditions associated with food allergy involving both IgE- and non-IgE-mediated mechanisms (3).

    A series of adverse reactions to foods do not involve an immune response and are not considered food allergies (4).

    These include metabolic disorders (for instance, lactose and alcohol intolerance), responses to pharmacologically athletic food components, as caffeine, theobromine in chocolate or tyramine in fermented cheeses, or toxic reactions. Toxic reactions to food can happen in any patient, if a sufficient quantity of the food is ingested; they are due to toxins in the food, e.g., to histamine in scombroid fish or bacterial toxins in food.

    While sometimes these, and other presumed food allergic reactions, are defined “food intolerances”, this term should not be used to define an allergic reaction (5).

    Host factors such as lactase deficiency, which are associated with lactose intolerance, or idiosyncratic responses may be responsible for other non-allergic reactions to foods.

    Underlying Mechanisms of Food Allergy

    Typical food allergies are IgE-mediated, but several reactions involve diverse immunologic mechanisms. These food allergies are defined as non–IgE-mediated or mixed IgE- and non–IgE-mediated.

    The symptoms of IgE-mediated, non-IgE–mediated, and mixed IgE- and non–IgE-mediated food allergy are presented in Table 13.

    IgE-mediated symptoms develop within minutes to hours of ingesting the food, non–IgE-mediated and mixed IgE- and non–IgE-mediated food allergies present with their symptoms several hours after the ingestion of the food.

    All these manifestations derive from a failure to develop or a breakdown of food tolerance, resulting in excessive production of food-specific IgE antibodies or in altered cellular events, leading to allergic reactions. Environmental influences and genetic factors of the host underlie the immunopathogenesis of food allergy and its manifestations. Some clinical studies own revised our understanding of the cause of food allergy.

    For example, functional genetic variants in the IL receptor b1, Toll-like receptor 9, and thymic stromal lymphopoietin genes and even IL-4 gene polymorphism own been associated with an increased risk of food sensitization (6). In the future, the elucidation of the gene-environment interactions will be crucial for understanding the food allergy pathogenesis. Microbiome, i.e., -omic, studies are an emerging field of interest to define allergy pathogenesis and, in a not too distant future, the microbiome could offer novel therapeutic possibilities (7).

    Epidemiology

    Food allergy is described as an increasing disease over time.

    It is generally accepted that food allergy affects approximately % of the general population, but the spread of prevalence data is wide, ranging from 1% to 10%. Precise determination of the prevalence is still one of the major problems with food allergy, considering that numerous factors influence the reported prevalence of food allergy. The varied factors include differing criteria for making food allergy diagnosis, study methodologies, geographic variation, ages, and dietary exposures to name a few. In European birth cohorts, the incidence ranges from % (United Kingdom) to % (Greece) (8).

    The most common foods, eaten separately or included as an ingredient, even in trace amounts (hidden food), that elicit hypersensitivity reactions are milk, egg, wheat, fish, and nuts.

    Despite the fact that up to % of newborn during the first years of life are diagnosed as allergic to cow's milk, recent European prevalence data repair the prevalence of cow’s milk allergy (CMA) to % (9).

    Within the EuroPrevall birth cohort, the mean adjusted incidence of hen’s egg allergy was % (10), while the Australian Healthnuts study reports a prevalence of 9% (11).

    The prevalence of peanut allergy among children in the United Kingdom, North America, and Australia has been reported doubled in 10 years and is approximately %, %, and % respectively.

    Fish allergy prevalence ranges from 0% to 7% and the prevalence of shellfish allergy from 0% to %, depending on the method used for diagnosis.

    The only study using food challenges reports a prevalence of fish allergy of 0% — % and a prevalence of shellfish allergy ranging between 0% and %. Fish allergy seems more frequent in Asia (12) than in Western countries (13).

    Epidemiological studies reveal that among food-allergic infants, approximately 80% will reach tolerance by the fifth birthday, but 35% of them may eventually develop hypersensitivity to other foods. Those with the highest IgE levels, with the most serious clinical manifestations (anaphylaxis and asthma), and with the wider co-sensitizations are less likely to overgrowth their food allergy.

    The natural history of food allergy also depends on the specific food sensitization, with children allergic to milk and egg displaying a better prognosis than those allergic to peanuts, tree nuts and fish(14).

    Cross-Reactivity and Food Allergens

    Component Resolved Diagnosis (CRD) elucidated the link between a severe allergy to pollen and the increase of oral allergy syndrome (OAS), exercise induced asthma and anaphylaxis when eating certain foods. Such reactions are due to cross-reactive allergens as pathogenesis related (PR), profilins, or lipid transfer proteins (LTP). These proteins are ubiquitous in pollens, plants, fruits and food.

    Individuals sensitive to home dust mites own been reported with oral allergy syndrome following ingestion of shellfish(15). Children with CMA may react to beef in up to 20% of cases, to goat’s milk in 98%, and to donkey milk in 20% of cases(16).

    IgE-Mediated Food-Related Disorders

    Skin Manifestations

    Acute urticaria and angioedema are the most frequent manifestation of food allergy. The onset of symptoms may be rapid, within minutes, following the ingestion of the offending food.

    Foods most often implicated include milk, fish, vegetables and fruits. In atopic dermatitis, also a frequent symptom of food allergy, immediate reactions can be followed by tardy cutaneous reactions.

    Gastrointestinal Tract

    Symptoms caused by immediate sensitivity in the gastrointestinal tract typically develop within minutes to 2 hours of ingesting the offending food. Symptoms can include lip, tongue and palatal pruritus and swelling, laryngeal oedema, nausea, abdominal cramping, vomiting and diarrhoea. Severe reactions can result in most or every symptoms associated with anaphylaxis.

    Oral allergy syndrome (OAS), a form of contact urticaria confined to the lips and oropharynx, most commonly occurs in pollen-allergic patients.

    Symptoms include oropharyngeal itching, with or without facial angioedema, and/or tingling of the lips, tongue, palate and throat.

    Respiratory Reactions

    Allergic rhinoconjunctivitis and asthma can happen following food challenge testing, but respiratory symptoms from food allergy in the absence of skin or gastrointestinal manifestations are rare. When respiratory symptoms happen following food challenge, both early- and late-phase IgE-mediated mechanisms are probably involved.

    Systemic reaction: Anaphylaxis

    Anaphylaxis is an explosive systemic reaction. About 50% of anaphylaxis reactions are due to food allergy. It occurs within few minutes to hours after food ingestion(17).

    Ninety per cent of patients experience skin (urticaria, angioedema) plus respiratory symptoms such as asthma, rhinitis or conjunctivitis; in 30% of the cases, they also develop gastrointestinal symptoms or hypotension, and shock and cardiac arrhythmias may happen. Every of this is caused by the massive release of mediators from mast cells and basophils.

    A form of anaphylaxis associated to food is the exercise-induced food-dependent anaphylaxis, occurring, generally, hours after ingestion of a food to which the individual is allergic. Food or exercise alone will not cause this reaction. Risk factors for food-induced anaphylaxis include asthma and previous allergic reactions to the causative food.

    Table 1.

    Specific Food-Induced Allergic Conditions3

    Non-IgE-Mediated Food Allergic Disorders

    Gastrointestinal

    Food allergy is also linked to manifestations of delayed hypersensitivity, partially IgE-mediated and partially non-IgE-mediated. It is implicated in Eosinophilic Esophagitis, Eosinophilic gastritis and gastroenteritis, food protein-induced enterocolitis syndrome, and allergic proctocolitis.

    Food protein –induced enterocolitis syndrome (FPIES)

    Primarily affects infants. In chronic forms, it presents as emesis, diarrhea, poor growth, and, in severe cases, with starvation and lethargy.

    In acute forms, or after re-istration of restricted foods, it may determine emesis, diarrhea, and hypotension, starting two hours following ingestion. Diarrhea may be bloody and may result in dehydration, especially in early infancy. It has been associated frequently to ingestion of cow's milk, soy, oat, wheat, and/or rice. Skin prick test to the suspected foods are generally negative, but IgE-mediated food allergy may be associated with FPIES as sometimes the two conditions co-exist or one form transforms into the another.

    International consensus guidelines own been developed for FPIES.(18)

    Food protein-induced allergic proctocolitis (FPIAP)

    FPIAP is a benign transient condition, typically starting in the first few months of life with bloody stools in well-appearing infants. About 60% of cases happen in breast-fed babies, the remainder in infants fed cow's milk or soy protein-based formulas.

    Rarely, dietary protein proctitis shows mild hypoalbuminaemia and peripheral eosinophilia. Bowel lesions are generally confined to distal large bowel; endoscopy reveals linear erosions and mucosal oedema with infiltration of eosinophils in the epithelium and lamina propria.

    Food-induced pulmonary haemosiderosis (Heiner's Syndrome)

    This extremely rare syndrome, affecting infants and young children, is characterized by recurrent episodes of pneumonia associated with pulmonary infiltrates, haemosiderosis, gastrointestinal blood loss, iron deficiency, anaemia, failure to thrive.

    It is due to cow's milk(19); the immunologic mechanism is still unknown.

    Mixed IgE and non-IgE reactions

    Eczema

    Although it is not, strictly speaking, an allergic disease, at least one-third of infants and young children with atopic eczema own IgE-mediated food allergy. Egg allergy is the most common food hypersensitivity in children with eczema. Appropriate diagnosis of food allergy and elimination of the offending allergen leads to significant clearing or improvement of eczematous lesions in numerous young children with eczema and food allergy. Food allergens may be triggers for some acute exacerbations (20).

    Allergic eosinophilic oesophagitis (EoE).

    This condition may present in children with a variety of nonspecific symptoms, e.g., feeding difficulty, nausea, vomiting, heartburn, and failure to thrive.

    Teenagers and adults are more likely to present with dysphagia and episodes of food impaction.

    Eighty percent of patients with eosinophilic esophagitis own symptoms similar to gastroesophageal reflux, which are refractory to anti-reflux therapy. In the case of infants, the vomitus often contains stringy mucus (similar to egg albumin). Patients may also present with food refusal, dysphagia, food impaction or abdominal pain. Food induced IgE-mediated allergy has been implicated in the pathogenesis in some patients.

    In eosinophilic esophagitis there may be years of unrecognized childhood subclinical disease or “silent” chronic inflammation before the diagnosis is made.(21)

    Allergic eosinophilic gastritis or gastroenteritis

    The exact cause of these disorders remains unknown although both IgE-mediated and T-cell-mediated reactions own been implicated. These conditions are characterized by infiltration of eosinophils in the mucosal, muscular and/or serosal layers of the stomach or little intestines. Patients present with postprandial nausea and vomiting, abdominal pain, diarrhea (occasionally steatorrhea) and weight loss in adults and failure to thrive in young infants.

    Diagnosis of Food Allergy

    The results of skin prick tests (SPT), IgE entire and specific antibodies, and patient histories are not predictive of true food allergy, as they are not capable to establish the causal and temporal relationship between the intake of the suspect food and the hypersensitivity reaction.

    The negative predictive accuracy of a skin prick test weal of < 3mm greater than the negative control is high, generally > 95%, and is strong evidence that the food may be consumed without severe, immediate food-allergic reactions. A positive SPT, even a weal of 3 mm or more, may be clinically irrelevant, as the patient may tolerate the ingested food. SPTs may also remain positive after the development of tolerance to the specific food.

    Specific IgE levels display a variable diagnostic accuracy according to the nature of the allergen, the studied population, the specific brand of the test.

    Using the most favorite diagnostic systems, in is conventionally accepted that kU/l is the cut-off level for a positive in-vitro test of specific IgE. Higher levels of specific IgE for food allergens may better correlate with clinical reactivity as evidenced by challenge testing. For this reason, decision points own been proposed. While valid in the studied populations, the worth of such decision points cannot be universal (see table below).

    A double blind, placebo-controlled food challenge (DBPCFC) is the preferred test to diagnose food allergy3,19.

    DBPCFC should be performed in specialist centers with shut supervision. Resuscitation facilities and overnight admission can be necessary in severe cases. DBPCFC is hard to organize in numerous clinical situations, and can be replaced by open challenges in numerous situations (when there is a minimal risk of untrue interpretations due to subjective factors). When a psychological reaction is strongly suspected, a single-blinded test may also be used (22, 23).

    The in vitro diagnostics can assist to identify cross-reactive allergens between pollen and foods, or foods and latex. Cross-reactive allergens include common lipid transfer proteins (LTPs), PR molecules, and profilin.

    Skin prick/puncture tests using commercial extracts to the implicated fruit are often negative, but a positive test may be obtained using a drop of unused juice from the incriminated fruit.

    The atopy patch test (APT) is an epicutaneous skin test in which allergens commonly associated with IgE reactions can be used, although patch testing is more commonly performed for metals such as nickel, which causes a positive patch test in nickel sensitive subjects. Although the pathogenic mechanisms of the APT own not been fully elucidated, a positive APT can predict a tardy phase reaction following oral food challenge.

    A positive APT may detect clinically relevant tardy phase eczematous or GI reactions in infants and children (24).

    What is the most common food allergy in uk

    This test is not useful for IgE-mediated food allergy. It is considered experimental in most parts of the world (25).

    Prevention of food allergy

    According to every the current guidelines, an baby with at least one first-degree relative (parent or sibling) with a history of allergic disease’ (26, 27) in specific allergic rhinitis, asthma, eczema, or food allergy (28, 29) is at greater risk for developing food allergy.

    The first proposed recommendation for a large-scale prevention of food allergy has been the use of hypoallergenic (HA) formulae in case of breastfeeding failure.

    This approach has reached the level of evidence to be included in the NIAID recommendations on food allergy prevention (30), but it has subsequently been questioned. (31) Earlier guidelines on allergy prevention recommended delayed exposure to solid foods, avoidance of allergenic foods, and did not include interventions aimed at promoting the infants’ immune tolerance (32). Emerging evidence, however, has led to a paradigm shift, supporting nutritional approaches such as appropriate timing of food exposure, and use of prebiotics and probiotics for allergy prevention.

    The Learning Early about Peanut (LEAP) study showed that early introduction of peanuts significantly decreased the frequency of peanut allergy among children at high risk, and modulated immune responses to peanuts (33). Hence, based on these findings, the National Institutes of Health (NIH) Guidelines for the Management and Prevention of Food Allergy subsequently recommended the introduction of peanut-containing foods to “high-risk” infants early in life ( months) (34).

    The World Allergy Organization (WAO)/McMaster Working Group Guidelines for Allergic Disease Prevention (GLAD-P) has also published GRADE recommendations on the use of probiotics and prebiotics for allergy prevention based on current available evidence.

    The guideline panel suggested using probiotics in pregnant and breastfeeding women whose children and infants are at high risk for developing allergy29. Probiotics own been shown by numerous studies to be effective in allergy prevention, particularly in reducing allergic eczema at a rate of 9 fewer cases per pregnant women (risk ratio [RR] ), 16 fewer cases per breastfeeding women (RR ), and 5 fewer cases per infants (RR ).

    Ultimately, the use of probiotics should be individualized and further studies are needed to assess their effect in preventing other types of allergy and the differences among the strains of the same species of probiotic bacteria.

    Concerning prebiotics, GLAD-P conditionally recommends prebiotic supplementation in non-exclusively breastfed infants, both at high and at low risk for developing allergy, but not in exclusively breastfed infants (35).

    These recommendations were largely based on a meta-analysis of available evidence showing that prebiotic supplementation reduces the risk of developing asthma or recurrent wheezing (RR: , 95 % CI: to ) and the risk of developing food allergy (RR: , 95 % CI: to ) (36). It has been proposed that these effects result from interactions between the gut microbiota and the gut mucosal immune system.

    GLAD-P provides no recommendation at this time on prebiotic use in pregnant and breastfeeding women, owing to the lack of evidence from experimental and observational studies.

    In the future, the GLAD-P guidelines may be expanded as more data from rigorously designed, adequately powered and well-executed trials become available.

    Recommendations on other interventional measures, such as vitamin D supplementation, in allergy prevention are negative (37).

    Treatment

    Food Allergen Avoidance

    The foods to which an individual is allergic should be avoided, as therapeutic intervention (tertiary prevention) in patients with food allergy. It must strike a precautionary equilibrium between the demands of prohibitive measures against allergy care and quality of life. Such a dynamic endpoint is hard to assess for efficacy and safety. Avoidance measures need to be tailored to the individual’s life and disease requirements must take account o the needs of growth, the prevention of anaphylaxis and, of the benefits expected of allergen avoidance itself.

    From the patient’s perspective, avoidance means meeting obstacles unshared by their non-allergic peers, thereby curtailing their quality of life.

    From the physician’s outlook, education, ensuring compliance and receptiveness of both patient and caregiver are major concerns. The role of the allergist is to review in a dialectical assessment these competing factors in concert with every parties concerned. Where avoidance of the implicated food may result in nutritional deficiency, dietary supplementation is necessary3.

    Processed foods may contain hidden proteins, e.g., milk, egg and soy proteins may be added to increase the protein content or enhance flavor.

    Peanuts and nut products are added to thicken and flavor sauces. Patients can be taught to identify hidden food components in processed foods. Commonly used ‘hidden' proteins are casein and lactose, derived from milk, and albumin from egg. To reveal hidden food allergens, food labelling is an issue of relevance to food allergic consumers of processed or pre-packaged foods. In the European Union, 12 food items are required by law to appear on the label: cereals containing gluten, crustaceans, egg, fish, peanut, soy, milk (including lactose), tree nuts, mustard, sesame seeds, celery, and sulfites >10 mg/kg (38).

    Similar legislation is in effect in the US, where the Food Allergen Labeling and Consumer Protection Act provides that every food products require an ingredient statement. In these countries, the legislation has altered industry practices in some significant aspects for milk, egg, peanut, tree nuts, shellfish, fish, soy and wheat. In other countries, hidden allergens can be exempt from specific labeling, and thus be inadvertently consumed by food allergic individuals. On both the sides of Atlantic, the regulatory problem is now the opposite concern, that is, whether too numerous foods containing trace amounts of these allergenic foods are being "overlabeled" and whether this would then potentially restrict potentially safe food choices for allergic consumers.

    In fact, the labeling regulations do not prescribe the indication of potential contaminants, but numerous manufacturers are now indicating, “may contain” as a warning of potential contaminations during food preparation (39).

    Pharmacological therapy

    Hypersensitivity reactions are often treated with medications. . Epinephrine is the only medication that is effective for the treatment of anaphylaxis. Additional medicatioons include H1 and H2 antihistamines, corticosteroids, and prostaglandin synthetase inhibitors These drugs are only symptomatic, do not modify the natural course of the disease, and sometimes own unacceptable side effects.

    Anti-IgE monoclonal antibodies therapy is licensed for use in asthma and for chronic urticaria in numerous countries, and studies are under way to determine if it has a role in the management of serious food allergies.

    Oral Immunotherapy

    Any desensitisation protocol to both reduce the risk of major reactions and avoid nutritional restrictions in children suffering from food allergy would be highly beneficial. The subcutaneous istration of native (40) or modified (41) peanut extracts was attempted in the past, but the shots induced systemic reactions or serious adverse effects.

    In the final years, the experience with oral immunotherapy has made this a common, accepted treatment in some countries. A recent systematic review concluded that oral immunotherapy is no longer experimental, but is ready for practical application (42). It should be applied to reduce the risk of inadvertent reactions, and not to modify the natural course of the disease (43). “Tolerance” in “desensitized” children disappears if the allergen is not ingested every day in therapeutic doses. However, research is ongoing and the future use of recombinant allergens (44), synthetic peptides (45),and epicutaneous therapy for desensitization in humans looks more promising (46).

    Natural history

    One of the most often asked parents’ questions is “How endless will my child’s food allergy last?” Given the present impossibility to modify the natural history of food allergy, the answer must take into account a series of factors.

    There is a relationship between symptom severity after ingestion and the likelihood of outgrowing the problem; the more severe the reaction, the less likely that the food allergy will be outgrown. Other factors, such as sIgE antibody level and age at diagnosis, own also been associated with prognosis of food allergy, although these associations are not invariably consistent across studies (47, 48, 49). Milk allergy’s half-life is approximately two years while egg allergy’s half-life is approximately four years. Peanut allergy, once considered to be a life-long condition, can resolve in up to 30% of cases (50).

    However, it is not possible to establish a half-life for a diagnosis of peanut allergy and tree nuts should still be considered as lifelong allergies.

    Similarly, fish allergy is considered a long-lasting condition and reports of recovery are rare (51). However, no study has evaluated the natural history of fish allergy in infants and fish should also be regarded as causing persistent allergies.

    While peanut, tree nut, fish and seafood allergy are mostly persistent conditions, little is known about the natural history of allergy to such staples as fruits, vegetables, cereals and meat.

    In food allergic children, tolerance must be tested by oral challenge at regular intervals.

    Often tolerance is not acquired suddenly, but there is a gradual increase of the doses tolerated at challenge. Even after years of apparent clinical tolerance, gastrointestinal symptoms of food allergy and reduced growth, . Epinephrine is the only medication that is effective for the treatment of anaphylaxis. own been reported (52).


    1. Johansson SG, Bieber T, Dahl R, et al: Revised nomenclature for allergy for global use: report of the Nomenclature Review Committee of the World Allergy Organization. J Allergy Clin Imunnol , –6

    2. Demoly P, Tanno LK, Akdis CA, Lau S, et al. Global classification and coding of hypersensitivity diseases – An EAACI – WAO survey, strategic paper and review.

    Allergy , –70

    3. Burks AW, Tang M, Sicherer S, et al. ICON: Food allergy. J Allergy Clin Immunol ,

    4. Boyce JA, Assa’ad A, Burks AW, Jones SM, Sampson HA, Wood RA, et al. Guidelines for the diagnosis and management of food allergy in the United States: report of the NIAID-sponsored expert panel. J. Allergy Clin Immunol ;(6 Suppl):S1–

    5. Dreborg S. Debates in allergy medicine: food intolerance does not exist.

    World Allergy Organ J. Dec 14;

    6. Xie J, Lotoski LC, Chooniedass R, et al. Elevated antigen-driven IL-9 responses are prominent in peanut allergic humans. PLoS One. ;7(10):e

    7. Prince BT, Mandel MJ, Nadeau K, Singh AM. Gut Microbiome and the Development of Food Allergy and Allergic Disease. Pediatric Clinics of North America. ;

    8. Grimshaw KE, Bryant T, Oliver EM, et al. Incidence and risk factors for food hypersensitivity in UK infants: results from a birth cohort study. Clin Transl Allergy. Jan 26;

    9. Schoemaker AA, Sprikkelman AB, Grimshaw KE, et al. Incidence and natural history of challenge-proven cow's milk allergy in European children — EuroPrevall birth cohort.

    Allergy. ;

    Xepapadaki P, Fiocchi A, Grabenhenrich L et al. Incidence and natural history of hen's egg allergy in the first 2 years of life — the EuroPrevall birth cohort study. Allergy. ;

    Koplin JJ, Osborne NJ, Wake M, et every. Can early introduction of egg prevent egg allergy in infants? A population-based study. J Allergy Clin Immunol. ;

    Thalayasingam M, Lee BW. Fish and shellfish allergy. Chem Immunol Allergy ;

    Sicherer SH, Muñoz-Furlong A, Sampson HA. Prevalence of seafood allergy in the United States sure by a random telephone survey. J Allergy Clin Immunol ;

    Kattan J.

    The Prevalence and Natural History of Food Allergy. Curr Allergy Asthma Rep. ;

    Matricardi PM, Kleine-Tebbe J, Hoffmann HJ. EAACI Molecular Allergology User's Guide. Pediatr Allergy Immunol May;27 Suppl

    Warren CM, Jhaveri S, Warrier MR, Smith B, Gupta RS. The epidemiology of milk allergy in US children. Ann Allergy Asthma Immunol ;

    Simons FE, Ebisawa M, Sanchez-Borges M, et al. update of the evidence base: World Allergy Organization anaphylaxis guidelines. World Allergy Organ J.

    Oct 28;

    Nowak-Węgrzyn A, Chehade M, Groetch M, et al. International Consensus Guidelines for the Diagnosis and Management of Food Protein-Induced Enterocolitis Syndrome: Workgroup Report of the Adverse Reactions to Foods Committee, American Academy of Allergy, Asthma, and Immunology. J Allergy Clin Immunol. Feb 3 [Epub ahead of print]

    Fiocchi A, Brozek J, Schunemann HJ, Bahna SL, von Berg A, Beyer K, et al. World Allergy Organization (WAO) Diagnosis and Rationale for Action against Cow’s Milk Allergy (DRACMA) Guidelines.

    WAO Journal ;

    Roerdink EM, Flokstra-de Blok BM, Blok JL, ET AL. Association of food allergy and atopic dermatitis exacerbations. Ann Allergy Asthma Immunol. ;

    Furuta GT, Katzka DA. Eosinophilic Esophagitis. N Engl J Med ;

    Komata T, Shukuya A, Imai T, Tachimoto H, Ebisawa M. Single blind food challenge using dried food powder nd Report. milk. Arerugi. ;

    Komata T, Shukuya A, Imai T, Tachimoto H, Ebisawa M. Single blind food challenge using dried food powderst report. Raw whole egg and egg yolk.

    Arerugi. ;

    Boonyaviwat O, Pacharn P, Jirapongsananuruk O, Vichyanond P, Visitsunthorn N. Role of atopy patch test for diagnosis of food allergy-related gastrointestinal symptoms in children. Pediatr Allergy Immunol. ;

    Edwards KP, Martinez BA. Atopy patch testing for foods: a review of the literature. Allergy Asthma Proc ;

    Greer FR, Sicherer SH, Burks AW et al; American Academy of Pediatrics Committee on Nutrition; American Academy of Pediatrics Section on Allergy and Immunology.

    Effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed rics. ;

    Muraro A, Halken S, Arshad SH, et al; EAACI Food Allergy and Anaphylaxis Guidelines Group. EAACI food allergy and anaphylaxis guidelines. Primary prevention of food allergy. Allergy. ;

    Boyce JA, Assa'ad A, Burks AW, et al. Guidelines for the diagnosis and management of food allergy in the United States: summary of the NIAID-sponsored expert panel report. J Allergy Clin Immunol. ;(6 Suppl):S

    Fiocchi A, Pawankar R, Cuello-Garcia C, et al.

    World Allergy Organization-McMaster University Guidelines for Allergic Disease Prevention (GLAD-P): Probiotics. World Allergy Organ J. ;

    Boyce JA, Assa'ad A, Burks AW, et al. Guidelines for the diagnosis and management of food allergy in the United States: summary of the NIAID-sponsored expert panel report. J Allergy Clin Immunol. ;(6 Suppl):S

    Boyle RJ, Ierodiakonou D, Khan T, et al. Hydrolysed formula and risk of allergic or autoimmune disease: systematic review and meta-analysis. BMJ. ;i

    Fiocchi A, Assa'ad A, Bahna S; Adverse Reactions to Foods Committee; American College of Allergy, Asthma and Immunology.

    Food allergy and the introduction of solid foods to infants: a consensus document. Adverse Reactions to Foods Committee, American College of Allergy, Asthma and Immunology. Ann Allergy Asthma Immunol. ;

    Du Toit G, Roberts G, Sayre PH, et al; LEAP Study Team. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med. ;

    Togias A, Cooper SF, Acebal ML, et al. Addendum guidelines for the prevention of peanut allergy in the United States. Report of the NIAID-sponsored expert panel.

    Allergy Asthma Clin Immunol. ;

    Cuello-Garcia CA, Fiocchi A, Pawankar R, Yepes-Nuñez JJ, Morgano GP, Zhang Y, Ahn K, Al-Hammadi S, Agarwal A, Gandhi S, Beyer K, Burks W, Canonica GW, Ebisawa M, Kamenwa R, Lee BW, Li H, Prescott S, Riva JJ, Rosenwasser L, Sampson H, Spigler M, Terracciano L, Vereda A, Waserman S, Schünemann HJ, Brożek JL. World Allergy Organization-McMaster University Guidelines for Allergic Disease Prevention (GLAD-P): Prebiotics. World Allergy Organ J. ;

    Cuello-Garcia CA, Brożek JL, Fiocchi A, Pawankar R, Yepes-Nuñez JJ, Terracciano L, Gandhi S, Agarwal A, Zhang Y, Schünemann HJ.

    Probiotics for the prevention of allergy: A systematic review and meta-analysis of randomized controlled trials. J Allergy Clin Immunol. ;

    Yepes-Nuñez JJ, Fiocchi A, Pawankar R, Cuello-Garcia CA, Zhang Y, Morgano GP, Ahn K, Al-Hammadi S, Agarwal A, Gandhi S, Beyer K, Burks W, Canonica GW, Ebisawa M, Kamenwa R, Lee BW, Li H, Prescott S, Riva JJ, Rosenwasser L, Sampson H, Spigler M, Terracciano L, Vereda A, Waserman S, Schünemann HJ, Brożek JL. World Allergy Organization-McMaster University Guidelines for Allergic Disease Prevention (GLAD-P): Vitamin D. World Allergy Organ J. ;

    Houben G, Burney P, Chan CH, Crevel R, Dubois A, et al.

    Prioritisation of allergenic foods with honor to public health relevance: Report from an ILSI Europe Food Allergy Task Force Expert Group. Food Chem Toxicol ;

    Allen KJ, Turner PJ, Pawankar R, Taylor S, Sicherer S, Lack G, Rosario N, Ebisawa M, Wong G, Mills EN, Beyer K, Fiocchi A, Sampson HA. Precautionary labelling of foods for allergen content: are we ready for a global framework? World Allergy Organ J. ;

    Nelson HS, Lahr J, Law R, Bock SA, Leung DYM. Treatment of anaphylactic sensitivity to peanuts by immunotherapy with injections of aqueous peanut extract. J Allergy Clin Immunol; 99 –

    Sampson HA. Immunological approaches to the treatment of food allergy.

    Pediatr Allergy Immunol;12 (suppl 14): 91 –96

    Nurmatov U, Dhami S, Arasi S, et al. Allergen immunotherapy for IgE-mediated food allergy: a systematic review and meta-analysis. Allergy. Jan 6. [Epub ahead of print]

    Dang TD, Peters RL, Allen KJ. Debates in allergy medicine: baked egg and milk do not accelerate tolerance to egg and milk. World Allergy Organ J. ; 26;

    Li XM, Srisvastava K, Grishin A, Huang C, Schofield BH, Burks AW, et al. Persistent protective effect of heat killed E. coli producing “engineered,” recombinant peanut proteins in a murine model of peanut allergy.

    J Allergy Clin Immunol ;

    Sicherer SH, Advances in anaphylaxis and hypersensitivity reactions to foods, drugs and insect venom. J Allergy Clin Immunol ; s

    Tordesillas L, Mondoulet L, Blazquez AB, et al. Epicutaneous immunotherapy induces gastrointestinal LAP(+) regulatory T cells and prevents food-induced anaphylaxis. J Allergy Clin Immunol ;

    Garcia-Ara MC, Boyano-Martinez MT, Diaz-Pena JM, Martin-Munoz MF, Martin-Esteban M. Cow's milk-specific immunoglobulin E levels as predictors of clinical reactivity in the follow-up of the cow's milk allergy infants. Clin Exp Allergy ;

    Shek LP, Soderstrom L, Ahlstedt S, Beyer K, Sampson HA.

    Determination of food specific IgE levels over time can predict the development of tolerance in cow's milk and hen's egg allergy. J Allergy Clin Immunol ;

    Fiocchi A, Terracciano L Bouygue GR, Veglia F, Sarratud T, Martelli A, Restani P. Incremental prognostic factors associated with cow's milk allergy outcomes in baby and kid referrals: the Milan Cow's Milk Allergy Cohort study. Ann Allergy Asthma Immunol ;

    Peters RL, Allen KJ, Dharmage SC,et al. Natural history of peanut allergy and predictors of resolution in the first 4 years of life: A population-based assessment.

    J Allergy Clin Immunol. ;

    Pite H, Prates S, Borrego LM, et al. Resolution of IgE-mediated fish allergy. Allergol Immunopathol (Madr). ;

    Kokkonen J, Tikkanen S, Savilahti R: Residual intestinal disease after milk allergy in infancy. J Pediatr Gastroenterol Nutr ;

    Competing Financial Interests Declaration

    Neither ENB nor CMS own any conflicts of interest, financial or otherwise.

    Competing Financial Interests Declaration

    Neither ENB nor CMS own any conflicts of interest, financial or otherwise.

    Definition and Classification

    The classification of allergic and hypersensitivity diseases was established by the European Academy of Allergy and Clinical Immunology (EAACI) and the World Allergy Organization (WAO) in (1).

    The definitions and concepts of allergic and hypersensitivity conditions beyond the allergy community own often created misunderstanding (2). For an optimal clarification:

    1. the term “atopy” is used when individuals own an IgE sensitization as documented by IgE antibodies in serum or by a positive skin prick test;
    2. “hypersensitivity” is defined as “conditions clinically resembling allergy that cause objectively reproducible symptoms or signs, initiated by exposure to a defined stimulus at a dose tolerated by normal subjects”, and
    3. “allergy” is defined “a hypersensitivity reaction initiated by proven or strongly suspected immunologic mechanisms”.

    Based on these definitions, a correct diagnosis of allergic disease must adhere to the following conditions:

    a) Compatible clinical history; and
    b) Positivity to in vivo and/or in vitro tests to prove underlying mechanism and etiology.

    The tests alone cannot be used because numerous people are sensitized (positive results to in vivo and/or in vitro tests), but not allergic (no reactions).

    Specifically for ‘food allergy’, this term is used when a causal relationship (ideally, with a specific immunological mechanism) has been defined.

    There are three wide groups of immune reactions: IgE-mediated, non-IgE-mediated and mixed. The IgE-mediated reactions are generally divided into immediate-onset reactions (arising up to 2 hours from the food ingestion) and immediate plus late-phase (in which the immediate onset symptoms are followed by prolonged or ongoing symptoms). Non-IgE-mediated reactions, which are poorly defined both clinically and scientifically, are believed to be generally T-cell-mediated.

    They are typically delayed in onset, and happen 4 to 28 hours after ingestion of the offending food(s). Mixed IgE and non-IgE mediated reaction are conditions associated with food allergy involving both IgE- and non-IgE-mediated mechanisms (3).

    A series of adverse reactions to foods do not involve an immune response and are not considered food allergies (4). These include metabolic disorders (for instance, lactose and alcohol intolerance), responses to pharmacologically athletic food components, as caffeine, theobromine in chocolate or tyramine in fermented cheeses, or toxic reactions.

    Toxic reactions to food can happen in any patient, if a sufficient quantity of the food is ingested; they are due to toxins in the food, e.g., to histamine in scombroid fish or bacterial toxins in food.

    While sometimes these, and other presumed food allergic reactions, are defined “food intolerances”, this term should not be used to define an allergic reaction (5). Host factors such as lactase deficiency, which are associated with lactose intolerance, or idiosyncratic responses may be responsible for other non-allergic reactions to foods.

    Underlying Mechanisms of Food Allergy

    Typical food allergies are IgE-mediated, but several reactions involve diverse immunologic mechanisms.

    These food allergies are defined as non–IgE-mediated or mixed IgE- and non–IgE-mediated.

    The symptoms of IgE-mediated, non-IgE–mediated, and mixed IgE- and non–IgE-mediated food allergy are presented in Table 13. IgE-mediated symptoms develop within minutes to hours of ingesting the food, non–IgE-mediated and mixed IgE- and non–IgE-mediated food allergies present with their symptoms several hours after the ingestion of the food.

    All these manifestations derive from a failure to develop or a breakdown of food tolerance, resulting in excessive production of food-specific IgE antibodies or in altered cellular events, leading to allergic reactions.

    Environmental influences and genetic factors of the host underlie the immunopathogenesis of food allergy and its manifestations. Some clinical studies own revised our understanding of the cause of food allergy. For example, functional genetic variants in the IL receptor b1, Toll-like receptor 9, and thymic stromal lymphopoietin genes and even IL-4 gene polymorphism own been associated with an increased risk of food sensitization (6). In the future, the elucidation of the gene-environment interactions will be crucial for understanding the food allergy pathogenesis.

    Microbiome, i.e., -omic, studies are an emerging field of interest to define allergy pathogenesis and, in a not too distant future, the microbiome could offer novel therapeutic possibilities (7).

    Epidemiology

    Food allergy is described as an increasing disease over time. It is generally accepted that food allergy affects approximately % of the general population, but the spread of prevalence data is wide, ranging from 1% to 10%. Precise determination of the prevalence is still one of the major problems with food allergy, considering that numerous factors influence the reported prevalence of food allergy.

    The varied factors include differing criteria for making food allergy diagnosis, study methodologies, geographic variation, ages, and dietary exposures to name a few. In European birth cohorts, the incidence ranges from % (United Kingdom) to % (Greece) (8).

    The most common foods, eaten separately or included as an ingredient, even in trace amounts (hidden food), that elicit hypersensitivity reactions are milk, egg, wheat, fish, and nuts.

    Despite the fact that up to % of newborn during the first years of life are diagnosed as allergic to cow's milk, recent European prevalence data repair the prevalence of cow’s milk allergy (CMA) to % (9).

    Within the EuroPrevall birth cohort, the mean adjusted incidence of hen’s egg allergy was % (10), while the Australian Healthnuts study reports a prevalence of 9% (11).

    The prevalence of peanut allergy among children in the United Kingdom, North America, and Australia has been reported doubled in 10 years and is approximately %, %, and % respectively.

    Fish allergy prevalence ranges from 0% to 7% and the prevalence of shellfish allergy from 0% to %, depending on the method used for diagnosis.

    The only study using food challenges reports a prevalence of fish allergy of 0% — % and a prevalence of shellfish allergy ranging between 0% and %. Fish allergy seems more frequent in Asia (12) than in Western countries (13).

    Epidemiological studies reveal that among food-allergic infants, approximately 80% will reach tolerance by the fifth birthday, but 35% of them may eventually develop hypersensitivity to other foods. Those with the highest IgE levels, with the most serious clinical manifestations (anaphylaxis and asthma), and with the wider co-sensitizations are less likely to overgrowth their food allergy.

    The natural history of food allergy also depends on the specific food sensitization, with children allergic to milk and egg displaying a better prognosis than those allergic to peanuts, tree nuts and fish(14).

    Cross-Reactivity and Food Allergens

    Component Resolved Diagnosis (CRD) elucidated the link between a severe allergy to pollen and the increase of oral allergy syndrome (OAS), exercise induced asthma and anaphylaxis when eating certain foods. Such reactions are due to cross-reactive allergens as pathogenesis related (PR), profilins, or lipid transfer proteins (LTP). These proteins are ubiquitous in pollens, plants, fruits and food.

    Individuals sensitive to home dust mites own been reported with oral allergy syndrome following ingestion of shellfish(15). Children with CMA may react to beef in up to 20% of cases, to goat’s milk in 98%, and to donkey milk in 20% of cases(16).

    IgE-Mediated Food-Related Disorders

    Skin Manifestations

    Acute urticaria and angioedema are the most frequent manifestation of food allergy.

    The onset of symptoms may be rapid, within minutes, following the ingestion of the offending food. Foods most often implicated include milk, fish, vegetables and fruits. In atopic dermatitis, also a frequent symptom of food allergy, immediate reactions can be followed by tardy cutaneous reactions.

    Gastrointestinal Tract

    Symptoms caused by immediate sensitivity in the gastrointestinal tract typically develop within minutes to 2 hours of ingesting the offending food. Symptoms can include lip, tongue and palatal pruritus and swelling, laryngeal oedema, nausea, abdominal cramping, vomiting and diarrhoea.

    Severe reactions can result in most or every symptoms associated with anaphylaxis.

    Oral allergy syndrome (OAS), a form of contact urticaria confined to the lips and oropharynx, most commonly occurs in pollen-allergic patients. Symptoms include oropharyngeal itching, with or without facial angioedema, and/or tingling of the lips, tongue, palate and throat.

    Respiratory Reactions

    Allergic rhinoconjunctivitis and asthma can happen following food challenge testing, but respiratory symptoms from food allergy in the absence of skin or gastrointestinal manifestations are rare.

    When respiratory symptoms happen following food challenge, both early- and late-phase IgE-mediated mechanisms are probably involved.

    Systemic reaction: Anaphylaxis

    Anaphylaxis is an explosive systemic reaction. About 50% of anaphylaxis reactions are due to food allergy. It occurs within few minutes to hours after food ingestion(17). Ninety per cent of patients experience skin (urticaria, angioedema) plus respiratory symptoms such as asthma, rhinitis or conjunctivitis; in 30% of the cases, they also develop gastrointestinal symptoms or hypotension, and shock and cardiac arrhythmias may happen. Every of this is caused by the massive release of mediators from mast cells and basophils.

    A form of anaphylaxis associated to food is the exercise-induced food-dependent anaphylaxis, occurring, generally, hours after ingestion of a food to which the individual is allergic.

    Food or exercise alone will not cause this reaction. Risk factors for food-induced anaphylaxis include asthma and previous allergic reactions to the causative food.

    Table 1. Specific Food-Induced Allergic Conditions3

    Non-IgE-Mediated Food Allergic Disorders

    Gastrointestinal

    Food allergy is also linked to manifestations of delayed hypersensitivity, partially IgE-mediated and partially non-IgE-mediated. It is implicated in Eosinophilic Esophagitis, Eosinophilic gastritis and gastroenteritis, food protein-induced enterocolitis syndrome, and allergic proctocolitis.

    Food protein –induced enterocolitis syndrome (FPIES)

    Primarily affects infants.

    In chronic forms, it presents as emesis, diarrhea, poor growth, and, in severe cases, with starvation and lethargy. In acute forms, or after re-istration of restricted foods, it may determine emesis, diarrhea, and hypotension, starting two hours following ingestion. Diarrhea may be bloody and may result in dehydration, especially in early infancy. It has been associated frequently to ingestion of cow's milk, soy, oat, wheat, and/or rice. Skin prick test to the suspected foods are generally negative, but IgE-mediated food allergy may be associated with FPIES as sometimes the two conditions co-exist or one form transforms into the another.

    International consensus guidelines own been developed for FPIES.(18)

    Food protein-induced allergic proctocolitis (FPIAP)

    FPIAP is a benign transient condition, typically starting in the first few months of life with bloody stools in well-appearing infants. About 60% of cases happen in breast-fed babies, the remainder in infants fed cow's milk or soy protein-based formulas.

    Rarely, dietary protein proctitis shows mild hypoalbuminaemia and peripheral eosinophilia. Bowel lesions are generally confined to distal large bowel; endoscopy reveals linear erosions and mucosal oedema with infiltration of eosinophils in the epithelium and lamina propria.

    Food-induced pulmonary haemosiderosis (Heiner's Syndrome)

    This extremely rare syndrome, affecting infants and young children, is characterized by recurrent episodes of pneumonia associated with pulmonary infiltrates, haemosiderosis, gastrointestinal blood loss, iron deficiency, anaemia, failure to thrive.

    It is due to cow's milk(19); the immunologic mechanism is still unknown.

    Mixed IgE and non-IgE reactions

    Eczema

    Although it is not, strictly speaking, an allergic disease, at least one-third of infants and young children with atopic eczema own IgE-mediated food allergy. Egg allergy is the most common food hypersensitivity in children with eczema. Appropriate diagnosis of food allergy and elimination of the offending allergen leads to significant clearing or improvement of eczematous lesions in numerous young children with eczema and food allergy.

    Food allergens may be triggers for some acute exacerbations (20).

    Allergic eosinophilic oesophagitis (EoE).

    This condition may present in children with a variety of nonspecific symptoms, e.g., feeding difficulty, nausea, vomiting, heartburn, and failure to thrive. Teenagers and adults are more likely to present with dysphagia and episodes of food impaction.

    Eighty percent of patients with eosinophilic esophagitis own symptoms similar to gastroesophageal reflux, which are refractory to anti-reflux therapy. In the case of infants, the vomitus often contains stringy mucus (similar to egg albumin).

    Patients may also present with food refusal, dysphagia, food impaction or abdominal pain. Food induced IgE-mediated allergy has been implicated in the pathogenesis in some patients. In eosinophilic esophagitis there may be years of unrecognized childhood subclinical disease or “silent” chronic inflammation before the diagnosis is made.(21)

    Allergic eosinophilic gastritis or gastroenteritis

    The exact cause of these disorders remains unknown although both IgE-mediated and T-cell-mediated reactions own been implicated. These conditions are characterized by infiltration of eosinophils in the mucosal, muscular and/or serosal layers of the stomach or little intestines.

    Patients present with postprandial nausea and vomiting, abdominal pain, diarrhea (occasionally steatorrhea) and weight loss in adults and failure to thrive in young infants.

    Diagnosis of Food Allergy

    The results of skin prick tests (SPT), IgE entire and specific antibodies, and patient histories are not predictive of true food allergy, as they are not capable to establish the causal and temporal relationship between the intake of the suspect food and the hypersensitivity reaction.

    The negative predictive accuracy of a skin prick test weal of < 3mm greater than the negative control is high, generally > 95%, and is strong evidence that the food may be consumed without severe, immediate food-allergic reactions. A positive SPT, even a weal of 3 mm or more, may be clinically irrelevant, as the patient may tolerate the ingested food. SPTs may also remain positive after the development of tolerance to the specific food.

    Specific IgE levels display a variable diagnostic accuracy according to the nature of the allergen, the studied population, the specific brand of the test.

    Using the most favorite diagnostic systems, in is conventionally accepted that kU/l is the cut-off level for a positive in-vitro test of specific IgE. Higher levels of specific IgE for food allergens may better correlate with clinical reactivity as evidenced by challenge testing. For this reason, decision points own been proposed. While valid in the studied populations, the worth of such decision points cannot be universal (see table below).

    A double blind, placebo-controlled food challenge (DBPCFC) is the preferred test to diagnose food allergy3,19. DBPCFC should be performed in specialist centers with shut supervision.

    Resuscitation facilities and overnight admission can be necessary in severe cases. DBPCFC is hard to organize in numerous clinical situations, and can be replaced by open challenges in numerous situations (when there is a minimal risk of untrue interpretations due to subjective factors). When a psychological reaction is strongly suspected, a single-blinded test may also be used (22, 23).

    The in vitro diagnostics can assist to identify cross-reactive allergens between pollen and foods, or foods and latex.

    Cross-reactive allergens include common lipid transfer proteins (LTPs), PR molecules, and profilin. Skin prick/puncture tests using commercial extracts to the implicated fruit are often negative, but a positive test may be obtained using a drop of unused juice from the incriminated fruit.

    The atopy patch test (APT) is an epicutaneous skin test in which allergens commonly associated with IgE reactions can be used, although patch testing is more commonly performed for metals such as nickel, which causes a positive patch test in nickel sensitive subjects.

    Although the pathogenic mechanisms of the APT own not been fully elucidated, a positive APT can predict a tardy phase reaction following oral food challenge. A positive APT may detect clinically relevant tardy phase eczematous or GI reactions in infants and children (24). This test is not useful for IgE-mediated food allergy. It is considered experimental in most parts of the world (25).

    Prevention of food allergy

    According to every the current guidelines, an baby with at least one first-degree relative (parent or sibling) with a history of allergic disease’ (26, 27) in specific allergic rhinitis, asthma, eczema, or food allergy (28, 29) is at greater risk for developing food allergy.

    The first proposed recommendation for a large-scale prevention of food allergy has been the use of hypoallergenic (HA) formulae in case of breastfeeding failure.

    This approach has reached the level of evidence to be included in the NIAID recommendations on food allergy prevention (30), but it has subsequently been questioned. (31) Earlier guidelines on allergy prevention recommended delayed exposure to solid foods, avoidance of allergenic foods, and did not include interventions aimed at promoting the infants’ immune tolerance (32). Emerging evidence, however, has led to a paradigm shift, supporting nutritional approaches such as appropriate timing of food exposure, and use of prebiotics and probiotics for allergy prevention. The Learning Early about Peanut (LEAP) study showed that early introduction of peanuts significantly decreased the frequency of peanut allergy among children at high risk, and modulated immune responses to peanuts (33).

    Hence, based on these findings, the National Institutes of Health (NIH) Guidelines for the Management and Prevention of Food Allergy subsequently recommended the introduction of peanut-containing foods to “high-risk” infants early in life ( months) (34).

    The World Allergy Organization (WAO)/McMaster Working Group Guidelines for Allergic Disease Prevention (GLAD-P) has also published GRADE recommendations on the use of probiotics and prebiotics for allergy prevention based on current available evidence. The guideline panel suggested using probiotics in pregnant and breastfeeding women whose children and infants are at high risk for developing allergy29.

    Probiotics own been shown by numerous studies to be effective in allergy prevention, particularly in reducing allergic eczema at a rate of 9 fewer cases per pregnant women (risk ratio [RR] ), 16 fewer cases per breastfeeding women (RR ), and 5 fewer cases per infants (RR ). Ultimately, the use of probiotics should be individualized and further studies are needed to assess their effect in preventing other types of allergy and the differences among the strains of the same species of probiotic bacteria.

    Concerning prebiotics, GLAD-P conditionally recommends prebiotic supplementation in non-exclusively breastfed infants, both at high and at low risk for developing allergy, but not in exclusively breastfed infants (35). These recommendations were largely based on a meta-analysis of available evidence showing that prebiotic supplementation reduces the risk of developing asthma or recurrent wheezing (RR: , 95 % CI: to ) and the risk of developing food allergy (RR: , 95 % CI: to ) (36). It has been proposed that these effects result from interactions between the gut microbiota and the gut mucosal immune system.

    GLAD-P provides no recommendation at this time on prebiotic use in pregnant and breastfeeding women, owing to the lack of evidence from experimental and observational studies.

    In the future, the GLAD-P guidelines may be expanded as more data from rigorously designed, adequately powered and well-executed trials become available.

    Recommendations on other interventional measures, such as vitamin D supplementation, in allergy prevention are negative (37).

    Treatment

    Food Allergen Avoidance

    The foods to which an individual is allergic should be avoided, as therapeutic intervention (tertiary prevention) in patients with food allergy. It must strike a precautionary equilibrium between the demands of prohibitive measures against allergy care and quality of life. Such a dynamic endpoint is hard to assess for efficacy and safety. Avoidance measures need to be tailored to the individual’s life and disease requirements must take account o the needs of growth, the prevention of anaphylaxis and, of the benefits expected of allergen avoidance itself.

    From the patient’s perspective, avoidance means meeting obstacles unshared by their non-allergic peers, thereby curtailing their quality of life.

    From the physician’s outlook, education, ensuring compliance and receptiveness of both patient and caregiver are major concerns. The role of the allergist is to review in a dialectical assessment these competing factors in concert with every parties concerned. Where avoidance of the implicated food may result in nutritional deficiency, dietary supplementation is necessary3.

    Processed foods may contain hidden proteins, e.g., milk, egg and soy proteins may be added to increase the protein content or enhance flavor.

    Peanuts and nut products are added to thicken and flavor sauces. Patients can be taught to identify hidden food components in processed foods. Commonly used ‘hidden' proteins are casein and lactose, derived from milk, and albumin from egg. To reveal hidden food allergens, food labelling is an issue of relevance to food allergic consumers of processed or pre-packaged foods. In the European Union, 12 food items are required by law to appear on the label: cereals containing gluten, crustaceans, egg, fish, peanut, soy, milk (including lactose), tree nuts, mustard, sesame seeds, celery, and sulfites >10 mg/kg (38).

    Similar legislation is in effect in the US, where the Food Allergen Labeling and Consumer Protection Act provides that every food products require an ingredient statement. In these countries, the legislation has altered industry practices in some significant aspects for milk, egg, peanut, tree nuts, shellfish, fish, soy and wheat. In other countries, hidden allergens can be exempt from specific labeling, and thus be inadvertently consumed by food allergic individuals. On both the sides of Atlantic, the regulatory problem is now the opposite concern, that is, whether too numerous foods containing trace amounts of these allergenic foods are being "overlabeled" and whether this would then potentially restrict potentially safe food choices for allergic consumers.

    In fact, the labeling regulations do not prescribe the indication of potential contaminants, but numerous manufacturers are now indicating, “may contain” as a warning of potential contaminations during food preparation (39).

    Pharmacological therapy

    Hypersensitivity reactions are often treated with medications. . Epinephrine is the only medication that is effective for the treatment of anaphylaxis. Additional medicatioons include H1 and H2 antihistamines, corticosteroids, and prostaglandin synthetase inhibitors These drugs are only symptomatic, do not modify the natural course of the disease, and sometimes own unacceptable side effects.

    Anti-IgE monoclonal antibodies therapy is licensed for use in asthma and for chronic urticaria in numerous countries, and studies are under way to determine if it has a role in the management of serious food allergies.

    Oral Immunotherapy

    Any desensitisation protocol to both reduce the risk of major reactions and avoid nutritional restrictions in children suffering from food allergy would be highly beneficial. The subcutaneous istration of native (40) or modified (41) peanut extracts was attempted in the past, but the shots induced systemic reactions or serious adverse effects.

    In the final years, the experience with oral immunotherapy has made this a common, accepted treatment in some countries. A recent systematic review concluded that oral immunotherapy is no longer experimental, but is ready for practical application (42). It should be applied to reduce the risk of inadvertent reactions, and not to modify the natural course of the disease (43). “Tolerance” in “desensitized” children disappears if the allergen is not ingested every day in therapeutic doses.

    However, research is ongoing and the future use of recombinant allergens (44), synthetic peptides (45),and epicutaneous therapy for desensitization in humans looks more promising (46).

    Natural history

    One of the most often asked parents’ questions is “How endless will my child’s food allergy last?” Given the present impossibility to modify the natural history of food allergy, the answer must take into account a series of factors. There is a relationship between symptom severity after ingestion and the likelihood of outgrowing the problem; the more severe the reaction, the less likely that the food allergy will be outgrown.

    Other factors, such as sIgE antibody level and age at diagnosis, own also been associated with prognosis of food allergy, although these associations are not invariably consistent across studies (47, 48, 49). Milk allergy’s half-life is approximately two years while egg allergy’s half-life is approximately four years. Peanut allergy, once considered to be a life-long condition, can resolve in up to 30% of cases (50). However, it is not possible to establish a half-life for a diagnosis of peanut allergy and tree nuts should still be considered as lifelong allergies.

    Similarly, fish allergy is considered a long-lasting condition and reports of recovery are rare (51). However, no study has evaluated the natural history of fish allergy in infants and fish should also be regarded as causing persistent allergies.

    While peanut, tree nut, fish and seafood allergy are mostly persistent conditions, little is known about the natural history of allergy to such staples as fruits, vegetables, cereals and meat.

    In food allergic children, tolerance must be tested by oral challenge at regular intervals.

    Often tolerance is not acquired suddenly, but there is a gradual increase of the doses tolerated at challenge. Even after years of apparent clinical tolerance, gastrointestinal symptoms of food allergy and reduced growth, . Epinephrine is the only medication that is effective for the treatment of anaphylaxis. own been reported (52).


    1. Johansson SG, Bieber T, Dahl R, et al: Revised nomenclature for allergy for global use: report of the Nomenclature Review Committee of the World Allergy Organization. J Allergy Clin Imunnol , –6

    2. Demoly P, Tanno LK, Akdis CA, Lau S, et al. Global classification and coding of hypersensitivity diseases – An EAACI – WAO survey, strategic paper and review.

    Allergy , –70

    3. Burks AW, Tang M, Sicherer S, et al. ICON: Food allergy. J Allergy Clin Immunol ,

    4. Boyce JA, Assa’ad A, Burks AW, Jones SM, Sampson HA, Wood RA, et al. Guidelines for the diagnosis and management of food allergy in the United States: report of the NIAID-sponsored expert panel. J. Allergy Clin Immunol ;(6 Suppl):S1–

    5. Dreborg S. Debates in allergy medicine: food intolerance does not exist.

    World Allergy Organ J. Dec 14;

    6. Xie J, Lotoski LC, Chooniedass R, et al. Elevated antigen-driven IL-9 responses are prominent in peanut allergic humans. PLoS One. ;7(10):e

    7. Prince BT, Mandel MJ, Nadeau K, Singh AM. Gut Microbiome and the Development of Food Allergy and Allergic Disease. Pediatric Clinics of North America. ;

    8. Grimshaw KE, Bryant T, Oliver EM, et al. Incidence and risk factors for food hypersensitivity in UK infants: results from a birth cohort study. Clin Transl Allergy. Jan 26;

    9. Schoemaker AA, Sprikkelman AB, Grimshaw KE, et al. Incidence and natural history of challenge-proven cow's milk allergy in European children — EuroPrevall birth cohort.

    Allergy. ;

    Xepapadaki P, Fiocchi A, Grabenhenrich L et al. Incidence and natural history of hen's egg allergy in the first 2 years of life — the EuroPrevall birth cohort study. Allergy. ;

    Koplin JJ, Osborne NJ, Wake M, et every. Can early introduction of egg prevent egg allergy in infants? A population-based study. J Allergy Clin Immunol. ;

    Thalayasingam M, Lee BW. Fish and shellfish allergy. Chem Immunol Allergy ;

    Sicherer SH, Muñoz-Furlong A, Sampson HA. Prevalence of seafood allergy in the United States sure by a random telephone survey. J Allergy Clin Immunol ;

    Kattan J.

    The Prevalence and Natural History of Food Allergy. Curr Allergy Asthma Rep. ;

    Matricardi PM, Kleine-Tebbe J, Hoffmann HJ. EAACI Molecular Allergology User's Guide. Pediatr Allergy Immunol May;27 Suppl

    Warren CM, Jhaveri S, Warrier MR, Smith B, Gupta RS. The epidemiology of milk allergy in US children. Ann Allergy Asthma Immunol ;

    Simons FE, Ebisawa M, Sanchez-Borges M, et al. update of the evidence base: World Allergy Organization anaphylaxis guidelines.

    World Allergy Organ J. Oct 28;

    Nowak-Węgrzyn A, Chehade M, Groetch M, et al. International Consensus Guidelines for the Diagnosis and Management of Food Protein-Induced Enterocolitis Syndrome: Workgroup Report of the Adverse Reactions to Foods Committee, American Academy of Allergy, Asthma, and Immunology. J Allergy Clin Immunol. Feb 3 [Epub ahead of print]

    Fiocchi A, Brozek J, Schunemann HJ, Bahna SL, von Berg A, Beyer K, et al. World Allergy Organization (WAO) Diagnosis and Rationale for Action against Cow’s Milk Allergy (DRACMA) Guidelines.

    WAO Journal ;

    Roerdink EM, Flokstra-de Blok BM, Blok JL, ET AL. Association of food allergy and atopic dermatitis exacerbations. Ann Allergy Asthma Immunol. ;

    Furuta GT, Katzka DA. Eosinophilic Esophagitis. N Engl J Med ;

    Komata T, Shukuya A, Imai T, Tachimoto H, Ebisawa M. Single blind food challenge using dried food powder nd Report. milk. Arerugi. ;

    Komata T, Shukuya A, Imai T, Tachimoto H, Ebisawa M. Single blind food challenge using dried food powderst report.

    Raw whole egg and egg yolk. Arerugi. ;

    Boonyaviwat O, Pacharn P, Jirapongsananuruk O, Vichyanond P, Visitsunthorn N. Role of atopy patch test for diagnosis of food allergy-related gastrointestinal symptoms in children. Pediatr Allergy Immunol. ;

    Edwards KP, Martinez BA. Atopy patch testing for foods: a review of the literature. Allergy Asthma Proc ;

    Greer FR, Sicherer SH, Burks AW et al; American Academy of Pediatrics Committee on Nutrition; American Academy of Pediatrics Section on Allergy and Immunology.

    Effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed rics. ;

    Muraro A, Halken S, Arshad SH, et al; EAACI Food Allergy and Anaphylaxis Guidelines Group. EAACI food allergy and anaphylaxis guidelines. Primary prevention of food allergy. Allergy. ;

    Boyce JA, Assa'ad A, Burks AW, et al.

    Guidelines for the diagnosis and management of food allergy in the United States: summary of the NIAID-sponsored expert panel report. J Allergy Clin Immunol. ;(6 Suppl):S

    Fiocchi A, Pawankar R, Cuello-Garcia C, et al. World Allergy Organization-McMaster University Guidelines for Allergic Disease Prevention (GLAD-P): Probiotics. World Allergy Organ J. ;

    Boyce JA, Assa'ad A, Burks AW, et al. Guidelines for the diagnosis and management of food allergy in the United States: summary of the NIAID-sponsored expert panel report. J Allergy Clin Immunol.

    ;(6 Suppl):S

    Boyle RJ, Ierodiakonou D, Khan T, et al. Hydrolysed formula and risk of allergic or autoimmune disease: systematic review and meta-analysis. BMJ. ;i

    Fiocchi A, Assa'ad A, Bahna S; Adverse Reactions to Foods Committee; American College of Allergy, Asthma and Immunology. Food allergy and the introduction of solid foods to infants: a consensus document. Adverse Reactions to Foods Committee, American College of Allergy, Asthma and Immunology. Ann Allergy Asthma Immunol. ;

    Du Toit G, Roberts G, Sayre PH, et al; LEAP Study Team. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med. ;

    Togias A, Cooper SF, Acebal ML, et al.

    Addendum guidelines for the prevention of peanut allergy in the United States. Report of the NIAID-sponsored expert panel. Allergy Asthma Clin Immunol. ;

    Cuello-Garcia CA, Fiocchi A, Pawankar R, Yepes-Nuñez JJ, Morgano GP, Zhang Y, Ahn K, Al-Hammadi S, Agarwal A, Gandhi S, Beyer K, Burks W, Canonica GW, Ebisawa M, Kamenwa R, Lee BW, Li H, Prescott S, Riva JJ, Rosenwasser L, Sampson H, Spigler M, Terracciano L, Vereda A, Waserman S, Schünemann HJ, Brożek JL. World Allergy Organization-McMaster University Guidelines for Allergic Disease Prevention (GLAD-P): Prebiotics. World Allergy Organ J. ;

    Cuello-Garcia CA, Brożek JL, Fiocchi A, Pawankar R, Yepes-Nuñez JJ, Terracciano L, Gandhi S, Agarwal A, Zhang Y, Schünemann HJ.

    Probiotics for the prevention of allergy: A systematic review and meta-analysis of randomized controlled trials. J Allergy Clin Immunol. ;

    Yepes-Nuñez JJ, Fiocchi A, Pawankar R, Cuello-Garcia CA, Zhang Y, Morgano GP, Ahn K, Al-Hammadi S, Agarwal A, Gandhi S, Beyer K, Burks W, Canonica GW, Ebisawa M, Kamenwa R, Lee BW, Li H, Prescott S, Riva JJ, Rosenwasser L, Sampson H, Spigler M, Terracciano L, Vereda A, Waserman S, Schünemann HJ, Brożek JL.

    World Allergy Organization-McMaster University Guidelines for Allergic Disease Prevention (GLAD-P): Vitamin D. World Allergy Organ J. ;

    Houben G, Burney P, Chan CH, Crevel R, Dubois A, et al. Prioritisation of allergenic foods with honor to public health relevance: Report from an ILSI Europe Food Allergy Task Force Expert Group. Food Chem Toxicol ;

    Allen KJ, Turner PJ, Pawankar R, Taylor S, Sicherer S, Lack G, Rosario N, Ebisawa M, Wong G, Mills EN, Beyer K, Fiocchi A, Sampson HA. Precautionary labelling of foods for allergen content: are we ready for a global framework?

    World Allergy Organ J. ;

    Nelson HS, Lahr J, Law R, Bock SA, Leung DYM. Treatment of anaphylactic sensitivity to peanuts by immunotherapy with injections of aqueous peanut extract. J Allergy Clin Immunol; 99 –

    Sampson HA. Immunological approaches to the treatment of food allergy. Pediatr Allergy Immunol;12 (suppl 14): 91 –96

    Nurmatov U, Dhami S, Arasi S, et al. Allergen immunotherapy for IgE-mediated food allergy: a systematic review and meta-analysis. Allergy. Jan 6. [Epub ahead of print]

    Dang TD, Peters RL, Allen KJ.

    Debates in allergy medicine: baked egg and milk do not accelerate tolerance to egg and milk. World Allergy Organ J. ; 26;

    Li XM, Srisvastava K, Grishin A, Huang C, Schofield BH, Burks AW, et al. Persistent protective effect of heat killed E. coli producing “engineered,” recombinant peanut proteins in a murine model of peanut allergy. J Allergy Clin Immunol ;

    Sicherer SH, Advances in anaphylaxis and hypersensitivity reactions to foods, drugs and insect venom. J Allergy Clin Immunol ; s

    Tordesillas L, Mondoulet L, Blazquez AB, et al.

    Epicutaneous immunotherapy induces gastrointestinal LAP(+) regulatory T cells and prevents food-induced anaphylaxis. J Allergy Clin Immunol ;

    Garcia-Ara MC, Boyano-Martinez MT, Diaz-Pena JM, Martin-Munoz MF, Martin-Esteban M. Cow's milk-specific immunoglobulin E levels as predictors of clinical reactivity in the follow-up of the cow's milk allergy infants. Clin Exp Allergy ;

    Shek LP, Soderstrom L, Ahlstedt S, Beyer K, Sampson HA. Determination of food specific IgE levels over time can predict the development of tolerance in cow's milk and hen's egg allergy.

    J Allergy Clin Immunol ;

    Fiocchi A, Terracciano L Bouygue GR, Veglia F, Sarratud T, Martelli A, Restani P. Incremental prognostic factors associated with cow's milk allergy outcomes in baby and kid referrals: the Milan Cow's Milk Allergy Cohort study. Ann Allergy Asthma Immunol ;

    Peters RL, Allen KJ, Dharmage SC,et al. Natural history of peanut allergy and predictors of resolution in the first 4 years of life: A population-based assessment. J Allergy Clin Immunol. ;

    Pite H, Prates S, Borrego LM, et al.

    Resolution of IgE-mediated fish allergy. Allergol Immunopathol (Madr). ;

    Kokkonen J, Tikkanen S, Savilahti R: Residual intestinal disease after milk allergy in infancy. J Pediatr Gastroenterol Nutr ;


    References

    • ^«List of 14 Allergens | Food Information | Food Legislation | Legislation | The Food Safety Authority of Ireland». . Retrieved
    • ^Allergies From Antibiotics |
    • ^CarbamazepineArchived at the Wayback Machine
    • ^What are the most serious side effects of Dilantin?: Basic |hived at the Wayback Machine
    • ^«Rare Meat Allergy Caused By Tick Bites May Be On The Rise».

      . 27 November

    • ^National Institutes of Health, NIAID Allergy Statistics
    • ^Conjunctivitis – allergic and infectious – information, symptoms and treatment |Bupa UK
    • ^Kaaber, K.; Veien, N. K.; Tjell, J. C. (). «Low nickel diet in the treatment of patients with chronic nickel dermatitis». British Journal of Dermatology. 98 (2): – doi/jtbx. PMID
    • ^«Two Types of Cosmetic Allergy».

      Archived from the original on Retrieved

    • ^Non-Steroidal Anti-Inflammatory Medicines (NSAIDs)
    • ^
    • ^Tetracycline –
    • ^ abcdRuethers, Thimo; Taki, Aya C.; Johnston, Elecia B.; Nugraha, Roni; Le, Thu T. K.; Kalic, Tanja; McLean, Thomas R.; Kamath, Sandip D.; Lopata, Andreas L. (August ). «Seafood allergy: A comprehensive review of fish and shellfish allergens». Molecular Immunology. : 28– doi/ ISSN PMID
    • ^Semen Allergy
    • ^«Banana — allergy information (InformAll: Communicating about Food Allergies — University of Manchester)».

      . Retrieved

    • ^Harlan Walker (). Oxford Symposium on Food & Cookery, Staplefoods: Proceedings. Oxford Symposium. ISBN. Retrieved March 7,
    • ^National Institutes of Health, NIAID Allergy Statistics Archived at the Wayback Machine
    • ^Semen Allergy Can Cause Flu-like Symptoms in Men |TopNews United States
    • ^
    • ^September CDA Journal – Toxicity and Allergy to Local AnesthesiaArchived at the Wayback Machine
    • ^Allergies From Antibiotics |
    • ^Getting Pregnant and Fertility Problems: Sperm Allergy
    • ^ abDog Allergy at American College of Allergy, Asthma & Immunology.

      References up to

    • ^United States Public Law C. Food Allergen Labelling And Consumer Protection Act of Public Law ;
    • ^ ab«Allergenic Foods and their Allergens, with links to Informall FARRP Nebraska».
    • ^Anticonvulsant Drug Therapy: Dilantin: Neurology: UI Health Topics
    • ^Xavier Basagaña, Jordi Sunyer, Manolis Kogevinas, Jan-Paul Zock, Enric Duran-Tauleria, Deborah Jarvis, Peter Burney, Josep Maria Anto, and on behalf of the European Community Respiratory Health Survey ().

      «Socioeconomic Status and Asthma Prevalence in Young Adults. The European Community Respiratory Health Survey». American Journal of Epidemiology. (2): – doi/aje/kwh PMIDCS1 maint: multiple names: authors list (link)

    • ^«Everything You Should Know About Wheat Allergy Diagnosis and Treatment». Verywell. Retrieved
    • ^MMS: Error
    • ^Grob, Martin; Reindl, Jürgen; Vieths, Stephan; Wüthrich, Brunello; Ballmer-Weber, Barbara K.

      (). «Heterogeneity of banana allergy: characterization of allergens in banana-allergic patients». Annals of Allergy, Asthma & Immunology. 89 (5): – doi/S(10)X.

      What is the most common food allergy in uk

      ISSN

    • ^Trileptal CMI approved
    • ^«JIACI · Journal of Investigational Allergology and Clinical Immunology». . Retrieved
    • ^«Allergy Society of South Africa – Wheat Allergy». Archived from the original on Retrieved
    • ^Hemmer, W.; Klug, C.; Swoboda, I. (). «Update on the bird-egg syndrome and genuine poultry meat allergy». Allergo Journal International. 25 (3): 68– doi/s PMC PMID
    • ^Akagawa M, Handoyo T, Ishii T, Kumazawa S, Morita N, Suyama K (). «Proteomic analysis of wheat flour allergens». J. Agric. Food Chem.

      55 (17): – doi/jfa. PMID

    • ^«Mold allergies, Mold allergy symptoms, What is mold allergy». Archived from the original on Retrieved
    • ^Permaul, P.; Stutius, L. M.; Sheehan, W. J.; Rangsithienchai, P.; Walter, J. E.; Twarog, F. J.; Young, M. C.; Scott, J. E.; Schneider, L. C.; Phipatanakul, W. (). «Sesame Allergy: Role of Specific IgE and Skin Prick Testing in Predicting Food Challenge Results». Allergy and Asthma Proceedings. 30 (6): – doi/aap PMC PMID
    • ^Tegretol (carbamazepine)
    • ^«Allergenic Foods and their Allergens, with links to Informall | FARRP | Nebraska».

      . Retrieved

    • ^«The Downside To Cosmetics – Cosmetic Allergy». Archived from the original on Retrieved
    • ^Dilantin Information from
    • ^«Lactose Intolerance or Milk Allergy: What’s the Difference?». . Retrieved
    • ^Thomas D. Horn (). Dermatology, Volume 2. Elsevier Health Sciences. p. ISBN.
    • ^‘Flu-like symptoms actually semen allergy’ – Times LIVE
    • ^Sicherer, Scott H.; Sampson, Hugh A.

      (). «Food allergy». Journal of Allergy and Clinical Immunology. (2): S–S doi/ ISSN PMID

    • ^Mold allergies, allergic response, and allergy symptoms
    • ^Gottfried Schmalz; Dorthe Arenholt Bindslev (). Biocompatibility of Dental Materials. Springer. ISBN. Retrieved March 5,
    • ^
    • ^Edward T. Bope; Rick D. Kellerman ().

      Conn’s Current Therapy Expert Consult. Elsevier Health Sciences. ISBN. Retrieved March 6,

    • Bolognia, Jean L.; et al. (). Dermatology. St. Louis: Mosby. ISBN.
    • ^Tong, Wai Sze; Yuen, Agatha WT; Wai, Christine YY; Leung, Nicki YH; Chu, Ka Hou; Leung, Patrick SC (). «Diagnosis of fish and shellfish allergies». Journal of Asthma and Allergy. 11: – doi/JAA.S ISSN PMC PMID
    • ^«Tomato — allergy information (InformAll: Communicating about Food Allergies — University of Manchester)». . Retrieved
    • ^«Lone Star Tick Bite Might Trigger Red Meat Allergy: Study». MedlinePlus.

      9 November Archived from the original on 15 November

    • ^Semen Allergy Can Be Treated, Study Shows |Daily Health Report
    • ^UPDATE 1-Semen allergy suspected in rare post-orgasm illness – AlertNetArchived at the Wayback Machine
    • ^National Institutes of Health, NIAID Allergy Statistics «Archived copy». Archived from the original on Retrieved CS1 maint: archived copy as title (link)
    • ^Vien, Niels K.; Kaaber, Knud (). «Nickel cobalt and chromium sensitivity in patients with pompholyx (dyshidrotic eczema)». Contact Dermatitis. 5 (6): –4. doi/jtbx. PMID
    • ^ Zacharisen MC, Elms NP, Kurup VP.

      Severe tomato allergy (Lycopersicon esculentum). Allergy Asthma Proc. ;23(2)

    • ^(99)/fulltext
    • James, William D.; et al. (). Andrews’ Diseases of the Skin: Clinical Dermatology. Saunders Elsevier. ISBN.
    1. Bolognia, Jean L.; et al. (). Dermatology. St. Louis: Mosby. ISBN.
    2. James, William D.; et al. (). Andrews’ Diseases of the Skin: Clinical Dermatology.

      Saunders Elsevier. ISBN.

    1. Bolognia, Jean L.; et al. (). Dermatology. St. Louis: Mosby. ISBN.
    2. James, William D.; et al. (). Andrews’ Diseases of the Skin: Clinical Dermatology. Saunders Elsevier. ISBN.


    RELATED VIDEO: